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| 0.9980 | CheY - dependent methylation of the asparagine receptor, ProteinMcpB , during chemotaxis in Bacillus subtilis. |
| 0.9196 | ProteinCheY - dependent methylation of the asparagine receptor, McpB, during chemotaxis in Bacillus subtilis. |
| 0.7265 | CheY - dependent Methylationmethylation of the asparagine receptor, McpB, during chemotaxis in Bacillus subtilis. |
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| 0.9987 | For the Gram - positive organism Bacillus subtilis, chemotaxis to the attractant asparagine is mediated by the chemoreceptor ProteinMcpB . |
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| 0.9935 | In this study, we show that rapid net demethylation of B. subtilis ProteinMcpB results in the immediate production of methanol, presumably due to the action of CheB. |
| 0.9912 | In this study, we show that rapid net demethylation of B. subtilis McpB results in the immediate production of methanol, presumably due to the action of ProteinCheB . |
| 0.6187 | In this study, we show that rapid net Methylationdemethylation of B. subtilis McpB results in the immediate production of methanol, presumably due to the action of CheB. |
| In this study, we show that rapid net Demethylationdemethylation of B. subtilis McpB results in the immediate production of methanol, presumably due to the action of CheB. | |
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| 0.9993 | We also show that net demethylation of ProteinMcpB occurs upon both addition and removal of asparagine. |
| 0.4519 | We also show that net Methylationdemethylation of McpB occurs upon both addition and removal of asparagine. |
| We also show that net Demethylationdemethylation of McpB occurs upon both addition and removal of asparagine. | |
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|---|---|
| 0.9983 | After each demethylation event, ProteinMcpB is remethylated to nearly prestimulus levels. |
| 0.8137 | After each demethylation event, McpB is Methylationremethylated to nearly prestimulus levels. |
| Score | Text |
|---|---|
| 0.9985 | Both remethylation events are attributable to ProteinCheR using S - adenosylmethionine as a substrate. |
| 0.8293 | Both Methylationremethylation events are attributable to CheR using S - adenosylmethionine as a substrate. |
| Both Catalysisremethylation events are attributable to CheR using S - adenosylmethionine as a substrate. | |
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| 0.9983 | Furthermore, we show that the remethylation of asparagine - bound McpB requires the response regulator, CheY - P, suggesting that ProteinCheY - P acts in a feedback mechanism to facilitate adaptation to positive stimuli during chemotaxis in B. subtilis. |
| 0.9972 | Furthermore, we show that the remethylation of asparagine - bound McpB requires the response regulator, ProteinCheY - P , suggesting that CheY - P acts in a feedback mechanism to facilitate adaptation to positive stimuli during chemotaxis in B. subtilis. |
| 0.9880 | Furthermore, we show that the remethylation of asparagine - bound ProteinMcpB requires the response regulator, CheY - P, suggesting that CheY - P acts in a feedback mechanism to facilitate adaptation to positive stimuli during chemotaxis in B. subtilis. |
| 0.8810 | Furthermore, we show that the Methylationremethylation of asparagine - bound McpB requires the response regulator, CheY - P, suggesting that CheY - P acts in a feedback mechanism to facilitate adaptation to positive stimuli during chemotaxis in B. subtilis. |
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| 0.9998 | This hypothesis is supported by two observations : a cheRBCD mutant is capable of transient excitation and subsequent oscillations that bring the flagellar rotational bias below the prestimulus value in the tethered cell assay, and the ProteincheRBCD mutant is capable of swarming in a Tryptone swarm plate. |
| 0.9998 | This hypothesis is supported by two observations : a ProteincheRBCD mutant is capable of transient excitation and subsequent oscillations that bring the flagellar rotational bias below the prestimulus value in the tethered cell assay, and the cheRBCD mutant is capable of swarming in a Tryptone swarm plate. |
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|---|---|
| 0.9647 | Transglycosylation reactions of Bacillus stearothermophilus Proteinmaltogenic amylase with acarbose and various acceptors. |
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| 0.9884 | It was observed that Bacillus stearothermophilus Proteinmaltogenic amylase cleaved the first glycosidic bond of acarbose to produce glucose and a pseudotrisaccharide ( PTS ) that was transferred to C - 6 of the glucose to give an alpha - ( 1 - - > 6 ) glycosidic linkage and the formation of isoacarbose. |
| 0.5754 | It was observed that Bacillus stearothermophilus maltogenic Proteinamylase cleaved the first glycosidic bond of acarbose to produce glucose and a pseudotrisaccharide ( PTS ) that was transferred to C - 6 of the glucose to give an alpha - ( 1 - - > 6 ) glycosidic linkage and the formation of isoacarbose. |
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| 0.9562 | We have purified and characterized a novel high molecular mass glycoprotein of P. chabaudi chabaudi Protein( Pc550gp ) that is transported to the erythrocyte membrane during the intraerythrocytic cycle. |
| Score | Text |
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| 0.9998 | Immuno fluorescence assays with polyclonal monospecific antibodies against ProteinPc550gp show that the protein to be localized in the periphery of young trophozoite stages i. e., on the plasma membrane or parasitophorous vacuole membrane. |
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| 0.9996 | Moreover, alkali extraction of purified infected erythrocyte membranes at mature stages of parasite development does not solubilize ProteinPc550gp , suggesting that it is an integral membrane protein. |
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| 0.9996 | In addition proteinase K digestion of intact infected host cells induced the disappearance of ProteinPc550gp . |
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| 0.9997 | Brefeldin A or low temperature ( 15 degrees C ) treatment did not affect the translocation of ProteinPc550gp from the parasite compartments to the erythrocyte membrane, indicating that the secretion of Pc550gp does not follow the classical transport pathway described in most eukaryotic cells. |
| 0.9996 | Brefeldin A or low temperature ( 15 degrees C ) treatment did not affect the translocation of Pc550gp from the parasite compartments to the erythrocyte membrane, indicating that the secretion of ProteinPc550gp does not follow the classical transport pathway described in most eukaryotic cells. |
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| 0.9991 | Here, we elucidate two essential steps and describe the roles played by the three translation factors EF - G, RRF, and ProteinIF3 . |
| 0.9982 | Here, we elucidate two essential steps and describe the roles played by the three translation factors EF - G, ProteinRRF , and IF3. |
| 0.9976 | Here, we elucidate two essential steps and describe the roles played by the three translation factors ProteinEF - G , RRF, and IF3. |
| Score | Text |
|---|---|
| 0.9985 | Release factor RF3 is known to catalyze the dissociation of RF1 or ProteinRF2 from ribosomes after polypeptide release. |
| 0.9982 | Release factor RF3 is known to catalyze the dissociation of ProteinRF1 or RF2 from ribosomes after polypeptide release. |
| 0.9927 | Release factor ProteinRF3 is known to catalyze the dissociation of RF1 or RF2 from ribosomes after polypeptide release. |
| Score | Text |
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| 0.9982 | We show that the next step is dissociation of 50S subunits from the 70S posttermination complex and that it is catalyzed by RRF and ProteinEF - G and requires GTP hydrolysis. |
| 0.9965 | We show that the next step is dissociation of 50S subunits from the 70S posttermination complex and that it is catalyzed by ProteinRRF and EF - G and requires GTP hydrolysis. |
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| 0.9987 | We show that this step requires initiation factor ProteinIF3 , whose role was previously thought to be restricted to promoting specific 30S initiation complex formation from free 30S subunits. |
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| 0.9796 | Effect of alternative Glycosylationglycosylation on insulin receptor processing. |
| 0.9509 | Effect of alternative glycosylation on Proteininsulin receptor processing. |
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| 0.9803 | The mature Proteininsulin receptor is a cell surface heterotetrameric glycoprotein composed of two alpha - and two beta - subunits. |
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| 0.9699 | To examine the importance of N - linked glycosylation on Proteininsulin receptor processing, we have used glucose deprivation as a tool to alter protein glycosylation. |
| 0.9253 | To examine the importance of GlycosylationN - linked glycosylation on insulin receptor processing, we have used glucose deprivation as a tool to alter protein glycosylation. |
| 0.9429 | To examine the importance of N - linked Glycosylationglycosylation on insulin receptor processing, we have used glucose deprivation as a tool to alter protein glycosylation. |
| 0.7012 | To examine the importance of GlycosylationN - linked glycosylation on insulin receptor processing, we have used glucose deprivation as a tool to alter protein glycosylation. |
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| 0.9978 | Co - precipitation assays provide evidence that the alternative proreceptor bound ProteinGRP78 , an endoplasmic reticulum molecular chaperone. |
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| 0.9765 | N - Glycosidase F treatment shows that the alternative proreceptor contained N - linked Entityoligosaccharides . |
| 0.9545 | N - Glycosidase F treatment shows that the alternative proreceptor contained GlycosylationN - linked oligosaccharides. |
| 0.9442 | ProteinN - Glycosidase F treatment shows that the alternative proreceptor contained N - linked oligosaccharides. |
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|---|---|
| 0.9492 | Yet, Proteinendoglycosidase H insensitivity indicates an aberrant oligosaccharide structure. |
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| 0.9669 | Upon refeeding cells that were initially deprived of glucose, the alternative proreceptor was processed to a higher molecular weight form and gained sensitivity to Proteinendoglycosidase H . |
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| 0.9993 | Thus far, the focus has been on acetylator genes ( NAT1, ProteinNAT2 ) and the activation of heterocyclic amines, carcinogens generated by cooking meat for prolonged periods at high temperature. |
| 0.9990 | Thus far, the focus has been on acetylator genes Protein( NAT1 , NAT2 ) and the activation of heterocyclic amines, carcinogens generated by cooking meat for prolonged periods at high temperature. |
| Score | Text |
|---|---|
| 0.9998 | Three case - control studies and one prospective study have shown a consistent trend towards higher risks for cancer with higher intakes of meat in rapid acetylators for NAT1, ProteinNAT2 or both genotypes. |
| 0.9998 | Three case - control studies and one prospective study have shown a consistent trend towards higher risks for cancer with higher intakes of meat in rapid acetylators for ProteinNAT1 , NAT2 or both genotypes. |
| Score | Text |
|---|---|
| 0.9997 | Other links between meat, cooking methods, metabolic genotypes and risk for cancer might include enhanced activation of polycyclic aromatic hydrocarbons and N - nitroso compounds by variant genotypes of CYP1A1 and ProteinCYP2E1 , respectively, and modulation by meat of the protective effect of the E4 allele of apolipoprotein E on risk for cancer of the proximal colon. |
| 0.9995 | Other links between meat, cooking methods, metabolic genotypes and risk for cancer might include enhanced activation of polycyclic aromatic hydrocarbons and N - nitroso compounds by variant genotypes of ProteinCYP1A1 and CYP2E1, respectively, and modulation by meat of the protective effect of the E4 allele of apolipoprotein E on risk for cancer of the proximal colon. |
| 0.9990 | Other links between meat, cooking methods, metabolic genotypes and risk for cancer might include enhanced activation of polycyclic aromatic hydrocarbons and N - nitroso compounds by variant genotypes of CYP1A1 and CYP2E1, respectively, and modulation by meat of the protective effect of the ProteinE4 allele of apolipoprotein E on risk for cancer of the proximal colon. |
| 0.9899 | Other links between meat, cooking methods, metabolic genotypes and risk for cancer might include enhanced activation of polycyclic aromatic hydrocarbons and N - nitroso compounds by variant genotypes of CYP1A1 and CYP2E1, respectively, and modulation by meat of the protective effect of the E4 allele of Proteinapolipoprotein E on risk for cancer of the proximal colon. |
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| 0.5464 | Differential expression of human Proteinlysyl hydroxylase genes, lysine hydroxylation, and cross - linking of type I collagen during osteoblastic differentiation in vitro. |
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| 0.9991 | We hypothesized that the tissue specificity of type I collagen cross - linking is, in part, due to the differential expression of lysyl hydroxylase genes ( Procollagen - lysine, 2 - oxyglutarate, 5 - dioxygenase 1, 2, and 3 [ PLOD1, ProteinPLOD2 , and PLOD3 ] ). |
| 0.9977 | We hypothesized that the tissue specificity of type I collagen cross - linking is, in part, due to the differential expression of lysyl hydroxylase genes ( Procollagen - lysine, 2 - oxyglutarate, 5 - dioxygenase 1, Protein2 , and 3 [ PLOD1, PLOD2, and PLOD3 ] ). |
| 0.9963 | We hypothesized that the tissue specificity of type I collagen cross - linking is, in part, due to the differential expression of lysyl hydroxylase genes ( Procollagen - lysine, 2 - oxyglutarate, 5 - dioxygenase 1, 2, and Protein3 [ PLOD1, PLOD2, and PLOD3 ] ). |
| 0.9954 | We hypothesized that the tissue specificity of type I collagen cross - linking is, in part, due to the differential expression of lysyl hydroxylase genes ( Procollagen - lysine, 2 - oxyglutarate, 5 - dioxygenase 1, 2, and 3 [ PLOD1, PLOD2, and ProteinPLOD3 ] ) . |
| 0.9297 | We hypothesized that the tissue specificity of type I collagen cross - linking is, in part, due to the differential expression of lysyl hydroxylase genes ( Procollagen - lysine, 2 - oxyglutarate, 5 - dioxygenase 1, 2, and 3 Protein[ PLOD1 , PLOD2, and PLOD3 ] ). |
| 0.7111 | We hypothesized that the tissue specificity of type I collagen cross - linking is, in part, due to the differential expression of lysyl hydroxylase genes Protein( Procollagen - lysine, 2 - oxyglutarate, 5 - dioxygenase 1 , 2, and 3 [ PLOD1, PLOD2, and PLOD3 ] ). |
| 0.9363 | We hypothesized that the tissue specificity of type I collagen cross - linking is, in part, due to the differential expression of lysyl hydroxylase genes ( Procollagen - lysine, 2 - oxyglutarate, 5 - dioxygenase 1, 2, and Protein3 [ PLOD1 , PLOD2, and PLOD3 ] ). |
| 0.8143 | We hypothesized that the tissue specificity of type I collagen cross - linking is, in part, due to the differential expression of lysyl hydroxylase genes ( Procollagen - lysine, 2 - oxyglutarate Protein, 5 - dioxygenase 1 , 2, and 3 [ PLOD1, PLOD2, and PLOD3 ] ). |
| 0.7823 | We hypothesized that the tissue specificity of type I collagen cross - linking is, in part, due to the differential expression of lysyl hydroxylase genes ( Procollagen - lysine Protein, 2 - oxyglutarate, 5 - dioxygenase 1 , 2, and 3 [ PLOD1, PLOD2, and PLOD3 ] ). |
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| 0.5110 | In addition, using the medium and cell layer / matrix fractions in these cultures, lysine Hydroxylationhydroxylation of type I collagen alpha chains and collagen cross - linking chemistries have been characterized. |
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| 0.9994 | High levels of ProteinPLOD1 and PLOD3 genes were expressed in both BMSCs and NSFs, and the expression levels did not change in the course of differentiation. |
| 0.9991 | High levels of PLOD1 and ProteinPLOD3 genes were expressed in both BMSCs and NSFs, and the expression levels did not change in the course of differentiation. |
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| 0.9996 | In contrast to the ProteinPLOD1 and PLOD3 genes, both cell types showed low PLOD2 gene expression in undifferentiated and early differentiated conditions. |
| 0.9995 | In contrast to the PLOD1 and PLOD3 genes, both cell types showed low ProteinPLOD2 gene expression in undifferentiated and early differentiated conditions. |
| 0.9994 | In contrast to the PLOD1 and ProteinPLOD3 genes, both cell types showed low PLOD2 gene expression in undifferentiated and early differentiated conditions. |
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| 0.9994 | However, fully differentiated BMSCs, but not NSFs, exhibited a significantly elevated level ( 6 - fold increase ) of ProteinPLOD2 mRNA. |
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| 0.9995 | The data suggests that ProteinPLOD2 expression is associated with lysine hydroxylation in the nontriple helical domains of collagen and, thus, could be partially responsible for the tissue - specific collagen cross - linking pattern. |
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| 0.9778 | Phenylalanine residues in the active site of Proteintyrosine hydroxylase : mutagenesis of Phe300 and Phe309 to alanine and metal ion - catalyzed hydroxylation of Phe300. |
| Score | Text |
|---|---|
| 0.9740 | Residues Phe300 and Phe309 of Proteintyrosine hydroxylase are located in the active site in the recently described three - dimensional structure of the enzyme, where they have been proposed to play roles in substrate binding. |
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| 0.9693 | Mutants of Proteintyrosine hydroxylase with alanine substituted for Phe300 or Phe309 have now been purified and characterized. |
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| 0.9572 | The F309A protein possesses 40 % less activity than wild - type Proteintyrosine hydroxylase in the production of DOPA, but full activity in the production of dihydropterin. |
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| 0.8885 | The K ( 6 - MPH4 ) value for F300A Proteintyrosine hydroxylase is twice the wild - type value. |
| 0.8410 | The K ( 6 - MPH4 ) value for ProteinF300A tyrosine hydroxylase is twice the wild - type value. |
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| 0.7185 | Characterization of Phe300 by MALDI - TOF mass spectrometry and amino acid sequencing showed that Hydroxylationhydroxylation only occurs in the isolated catalytic domain after incubation with a large excess of 7, 8 - dihydropterin, DTT, and Fe ( 2 + ). |
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| 0.9967 | Development of an enzyme - linked immunosorbent assay, using a monoclonal antibody against Proteinalpha2 - macroglobulin , for the diagnosis of systemic lupus erythematosus. |
| Score | Text |
|---|---|
| 0.9908 | OBJECTIVES : To develop an enzyme - linked immunosorbent assay ( ELISA ) using a monoclonal antibody ( mab ) directed against abnormally Glycosylationglycosylated serum alpha2 - macroglobulin ( alpha2 - M ) from patients with systemic lupus erythematosus ( SLE ). |
| 0.9501 | OBJECTIVES : To develop an enzyme - linked immunosorbent assay ( ELISA ) using a monoclonal antibody ( mab ) directed against abnormally glycosylated serum alpha2 - macroglobulin Protein( alpha2 - M ) from patients with systemic lupus erythematosus ( SLE ). |
| 0.8773 | OBJECTIVES : To develop an enzyme - linked immunosorbent assay ( ELISA ) using a monoclonal antibody ( mab ) directed against abnormally glycosylated serum Proteinalpha2 - macroglobulin ( alpha2 - M ) from patients with systemic lupus erythematosus ( SLE ). |
| Score | Text |
|---|---|
| 0.9948 | DESIGN AND METHODS : Serum alpha2 - M purified by HPLC from patients with SLE was injected in a Balb / c, CB6 F1 female mouse and hybrid cell lines were screened using Proteinalpha2 - M Glu - C fragments derived from SLE and normal donors ( NHS ). |
| 0.9917 | DESIGN AND METHODS : Serum Proteinalpha2 - M purified by HPLC from patients with SLE was injected in a Balb / c, CB6 F1 female mouse and hybrid cell lines were screened using alpha2 - M Glu - C fragments derived from SLE and normal donors ( NHS ). |
| Score | Text |
|---|---|
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| 0.9977 | RESULTS : The affinity of the mab for Proteinalpha2 - M from SLE, but not from the other diseases, was higher compared to NHS, as demonstrated by immunoblotting and ELISA. |
| Score | Text |
|---|---|
| 0.9920 | CONCLUSIONS : The ELISA was capable of recognizing changes of Glycosylationglycosylation of alpha2 - M in SLE and may be useful for its differential diagnosis. |
| 0.9905 | CONCLUSIONS : The ELISA was capable of recognizing changes of glycosylation of Proteinalpha2 - M in SLE and may be useful for its differential diagnosis. |
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| 0.9996 | These reactions are catalyzed by a dedicated methyltransferase ProteinCheR and a dedicated methylesterase CheB. |
| 0.9987 | These reactions are catalyzed by a dedicated methyltransferase CheR and a dedicated methylesterase ProteinCheB . |
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| 0.9996 | We investigated the action of ProteinCheB and its activated form, phospho - CheB, on a truncated form of the aspartate receptor of Escherichia coli that was missing the last 5 aa of the intact receptor. |
| 0.9901 | We investigated the action of CheB and its activated form, Proteinphospho - CheB , on a truncated form of the aspartate receptor of Escherichia coli that was missing the last 5 aa of the intact receptor. |
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| 0.9997 | ProteinCheB bound specifically to an affinity column carrying the isolated pentapeptide, implying that in the intact receptor the pentapeptide serves as a docking site for the methylesterase / deamidase and that the truncated receptor was inefficiently modified because the enzyme could not dock. |
| 0.7522 | CheB bound specifically to an affinity column carrying the isolated pentapeptide, implying that in the intact receptor the pentapeptide serves as a docking site for the Proteinmethylesterase / deamidase and that the truncated receptor was inefficiently modified because the enzyme could not dock. |
| Score | Text |
|---|---|
| 0.9998 | It is striking that the same pentapeptide serves as an activity - enhancing docking site for the methyltransferase ProteinCheR , the other enzyme involved in adaptational covalent modification of chemoreceptors. |
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| 0.9877 | We investigated the kinetics of mRNA induction, demethylation, and remethylation of the Proteinp16 promoter and second - exon CpG islands in T24 cells after 5 - aza - 2'- deoxycytidine ( 5 - Aza - CdR ) treatment to explore the relationship between CpG island methylation and gene transcription. |
| 0.9588 | We investigated the kinetics of mRNA induction, demethylation, and remethylation of the p16 Entitypromoter and second - exon CpG islands in T24 cells after 5 - aza - 2'- deoxycytidine ( 5 - Aza - CdR ) treatment to explore the relationship between CpG island methylation and gene transcription. |
| 0.9485 | We investigated the kinetics of mRNA induction, demethylation, and remethylation of the p16 promoter and second - exon CpG islands in T24 cells after 5 - aza - 2'- deoxycytidine ( 5 - Aza - CdR ) treatment to explore the relationship between CpG island DNA_methylationmethylation and gene transcription. |
| 0.9262 | We investigated the kinetics of mRNA induction, demethylation, and DNA_methylationremethylation of the p16 promoter and second - exon CpG islands in T24 cells after 5 - aza - 2'- deoxycytidine ( 5 - Aza - CdR ) treatment to explore the relationship between CpG island methylation and gene transcription. |
| 0.7222 | We investigated the kinetics of mRNA induction, demethylation, and remethylation of the p16 promoter and second - exon CpG islands in T24 cells after 5 - aza - 2'- deoxycytidine ( 5 - Aza - CdR ) treatment to explore the relationship between EntityCpG island methylation and gene transcription. |
| 0.7088 | We investigated the kinetics of mRNA induction, demethylation, and remethylation of the p16 promoter and Entitysecond - exon CpG islands in T24 cells after 5 - aza - 2'- deoxycytidine ( 5 - Aza - CdR ) treatment to explore the relationship between CpG island methylation and gene transcription. |
| 0.7960 | We investigated the kinetics of mRNA induction, demethylation, and remethylation of the p16 promoter and second - exon EntityCpG islands in T24 cells after 5 - aza - 2'- deoxycytidine ( 5 - Aza - CdR ) treatment to explore the relationship between CpG island methylation and gene transcription. |
| 0.6599 | We investigated the kinetics of mRNA induction, DNA_methylationdemethylation , and remethylation of the p16 promoter and second - exon CpG islands in T24 cells after 5 - aza - 2'- deoxycytidine ( 5 - Aza - CdR ) treatment to explore the relationship between CpG island methylation and gene transcription. |
| 0.5525 | We investigated the kinetics of mRNA induction, demethylation, and remethylation of the p16 promoter and second - exon CpG islands in T24 cells after 5 - aza - 2'- deoxycytidine ( 5 - Aza - CdR ) treatment to explore the relationship between EntityCpG island methylation and gene transcription. |
| We investigated the kinetics of mRNA induction, DNA_demethylationdemethylation , and remethylation of the p16 promoter and second - exon CpG islands in T24 cells after 5 - aza - 2'- deoxycytidine ( 5 - Aza - CdR ) treatment to explore the relationship between CpG island methylation and gene transcription. | |
| Score | Text |
|---|---|
| 0.9813 | The rates of remethylation of both CpG islands were associated with time but not with the rate of cell division, and remethylation of the p16 exon 2 CpG island occurred at a higher rate than that of the Proteinp16 promoter. |
| 0.9664 | The rates of remethylation of both CpG islands were associated with time but not with the rate of cell division, and DNA_methylationremethylation of the p16 exon 2 CpG island occurred at a higher rate than that of the p16 promoter. |
| 0.9639 | The rates of remethylation of both CpG islands were associated with time but not with the rate of cell division, and remethylation of the Proteinp16 exon 2 CpG island occurred at a higher rate than that of the p16 promoter. |
| 0.9048 | The rates of remethylation of both CpG islands were associated with time but not with the rate of cell division, and remethylation of the p16 exon 2 CpG island occurred at a higher rate than that of the p16 Entitypromoter . |
| 0.5281 | The rates of remethylation of both CpG islands were associated with time but not with the rate of cell division, and remethylation of the p16 Entityexon 2 CpG island occurred at a higher rate than that of the p16 promoter. |
| 0.9509 | The rates of DNA_methylationremethylation of both CpG islands were associated with time but not with the rate of cell division, and remethylation of the p16 exon 2 CpG island occurred at a higher rate than that of the p16 promoter. |
| 0.6523 | The rates of remethylation of both CpG islands were associated with time but not with the rate of cell division, and remethylation of the p16 exon 2 EntityCpG island occurred at a higher rate than that of the p16 promoter. |
| 0.5021 | The rates of remethylation of both EntityCpG islands were associated with time but not with the rate of cell division, and remethylation of the p16 exon 2 CpG island occurred at a higher rate than that of the p16 promoter. |
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| 0.9825 | The kinetics of DNA_methylationremethylation of the p16 exon 2, PAX - 6 exon 5, c - ABL exon 11, and MYF - 3 exon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are hypermethylated in T24 cells. |
| 0.9814 | The kinetics of remethylation of the p16 exon 2, PAX - 6 exon 5, c - ABL exon 11, and MYF - 3 exon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are DNA_methylationhypermethylated in T24 cells. |
| 0.9756 | The kinetics of remethylation of the Proteinp16 exon 2, PAX - 6 exon 5, c - ABL exon 11, and MYF - 3 exon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are hypermethylated in T24 cells. |
| 0.9712 | The kinetics of remethylation of the p16 exon 2, PAX - 6 exon 5, c - ABL exon 11, and ProteinMYF - 3 exon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are hypermethylated in T24 cells. |
| 0.9666 | The kinetics of remethylation of the p16 exon 2, PAX - 6 exon 5, Proteinc - ABL exon 11, and MYF - 3 exon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are hypermethylated in T24 cells. |
| 0.9610 | The kinetics of remethylation of the p16 exon 2, ProteinPAX - 6 exon 5, c - ABL exon 11, and MYF - 3 exon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are hypermethylated in T24 cells. |
| 0.9118 | The kinetics of remethylation of the p16 exon 2, PAX - 6 Entityexon 5 , c - ABL exon 11, and MYF - 3 exon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are hypermethylated in T24 cells. |
| 0.9040 | The kinetics of remethylation of the p16 exon 2, PAX - 6 exon 5, c - ABL Entityexon 11 , and MYF - 3 exon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are hypermethylated in T24 cells. |
| 0.8757 | The kinetics of remethylation of the p16 Entityexon 2 , PAX - 6 exon 5, c - ABL exon 11, and MYF - 3 exon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are hypermethylated in T24 cells. |
| 0.8204 | The kinetics of remethylation of the p16 exon 2, PAX - 6 exon 5, c - ABL exon 11, and MYF - 3 Entityexon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are hypermethylated in T24 cells. |
| 0.5206 | The kinetics of remethylation of the p16 exon 2, PAX - 6 Entityexon 5, c - ABL exon 11, and MYF - 3 exon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are hypermethylated in T24 cells. |
| 0.5121 | The kinetics of remethylation of the p16 exon 2, PAX - 6 exon 5, c - ABL exon 11, and MYF - 3 Entityexon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are hypermethylated in T24 cells. |
| Score | Text |
|---|---|
| 0.9971 | Remethylation occurred most rapidly in the p16, PAX - 6, and Proteinc - ABL genes, shown to be transcribed prior to drug treatment. |
| 0.9960 | Remethylation occurred most rapidly in the Proteinp16 , PAX - 6, and c - ABL genes, shown to be transcribed prior to drug treatment. |
| 0.9942 | Remethylation occurred most rapidly in the p16, ProteinPAX - 6 , and c - ABL genes, shown to be transcribed prior to drug treatment. |
| 0.9563 | DNA_methylationRemethylation occurred most rapidly in the p16, PAX - 6, and c - ABL genes, shown to be transcribed prior to drug treatment. |
| Score | Text |
|---|---|
| 0.9716 | These regions also exhibited higher levels of DNA_methylationremethylation in single - cell clones and subclones derived from 5 - Aza - CdR - treated T24 cells. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9936 | Also, marked relationship of microsatellite instability ( MSI ) and DNA methylation has been reported in sporadic colorectal cancer, which is a result of epigenetic inactivation of ProteinhMLH1 in association of promoter hypermethylation. |
| 0.9859 | Also, marked relationship of microsatellite instability ( MSI ) and DNA methylation has been reported in sporadic colorectal cancer, which is a result of epigenetic inactivation of hMLH1 in association of promoter DNA_methylationhypermethylation . |
| 0.9826 | Also, marked relationship of microsatellite instability ( MSI ) and DNA methylation has been reported in sporadic colorectal cancer, which is a result of epigenetic inactivation of hMLH1 in association of Entitypromoter hypermethylation. |
| Score | Text |
|---|---|
| 0.9943 | In the present study, we investigated the 5'CpG island hypermethylation of hMLH1, E - cadherin and Proteinp16 in 61 primary gastric cancers ( GCs ) by using combined bisulfite restriction analysis ( COBRA ) and methylation - specific PCR ( MSP ), and their MSI status. |
| 0.9925 | In the present study, we investigated the 5'CpG island hypermethylation of hMLH1, ProteinE - cadherin and p16 in 61 primary gastric cancers ( GCs ) by using combined bisulfite restriction analysis ( COBRA ) and methylation - specific PCR ( MSP ), and their MSI status. |
| 0.9907 | In the present study, we investigated the 5'CpG island DNA_methylationhypermethylation of hMLH1, E - cadherin and p16 in 61 primary gastric cancers ( GCs ) by using combined bisulfite restriction analysis ( COBRA ) and methylation - specific PCR ( MSP ), and their MSI status. |
| 0.9872 | In the present study, we investigated the 5'CpG island hypermethylation of ProteinhMLH1 , E - cadherin and p16 in 61 primary gastric cancers ( GCs ) by using combined bisulfite restriction analysis ( COBRA ) and methylation - specific PCR ( MSP ), and their MSI status. |
| 0.8857 | In the present study, we investigated the Entity5'CpG island hypermethylation of hMLH1, E - cadherin and p16 in 61 primary gastric cancers ( GCs ) by using combined bisulfite restriction analysis ( COBRA ) and methylation - specific PCR ( MSP ), and their MSI status. |
| 0.8781 | In the present study, we investigated the 5 ' EntityCpG island hypermethylation of hMLH1, E - cadherin and p16 in 61 primary gastric cancers ( GCs ) by using combined bisulfite restriction analysis ( COBRA ) and methylation - specific PCR ( MSP ), and their MSI status. |
| 0.5562 | In the present study, we investigated the Entity5'CpG island hypermethylation of hMLH1, E - cadherin and p16 in 61 primary gastric cancers ( GCs ) by using combined bisulfite restriction analysis ( COBRA ) and methylation - specific PCR ( MSP ), and their MSI status. |
| 0.5354 | In the present study, we investigated the 5 ' EntityCpG island hypermethylation of hMLH1, E - cadherin and p16 in 61 primary gastric cancers ( GCs ) by using combined bisulfite restriction analysis ( COBRA ) and methylation - specific PCR ( MSP ), and their MSI status. |
| Score | Text |
|---|---|
| 0.9895 | Of 61 GCs investigated, 5 ( 8. 1 % ) tumors presented hMLH1 methylation, 16 ( 26. 2 % ) and 25 ( 40. 9 % ) showed ProteinE - cadherin and p16 methylation respectively, and 8 ( 13. 1 % ) presented high - frequency MSI ( MSI - H ). |
| 0.9870 | Of 61 GCs investigated, 5 ( 8. 1 % ) tumors presented hMLH1 DNA_methylationmethylation , 16 ( 26. 2 % ) and 25 ( 40. 9 % ) showed E - cadherin and p16 methylation respectively, and 8 ( 13. 1 % ) presented high - frequency MSI ( MSI - H ). |
| 0.9851 | Of 61 GCs investigated, 5 ( 8. 1 % ) tumors presented ProteinhMLH1 methylation, 16 ( 26. 2 % ) and 25 ( 40. 9 % ) showed E - cadherin and p16 methylation respectively, and 8 ( 13. 1 % ) presented high - frequency MSI ( MSI - H ). |
| 0.9844 | Of 61 GCs investigated, 5 ( 8. 1 % ) tumors presented hMLH1 methylation, 16 ( 26. 2 % ) and 25 ( 40. 9 % ) showed E - cadherin and p16 DNA_methylationmethylation respectively, and 8 ( 13. 1 % ) presented high - frequency MSI ( MSI - H ). |
| 0.9795 | Of 61 GCs investigated, 5 ( 8. 1 % ) tumors presented hMLH1 methylation, 16 ( 26. 2 % ) and 25 ( 40. 9 % ) showed E - cadherin and Proteinp16 methylation respectively, and 8 ( 13. 1 % ) presented high - frequency MSI ( MSI - H ). |
| 0.8182 | Of 61 GCs investigated, 5 ( 8. 1 % ) tumors presented hMLH1 methylation, 16 ( 26. 2 % ) and 25 ( 40. 9 % ) showed E - cadherin and DNA_methylationp16 methylation respectively, and 8 ( 13. 1 % ) presented high - frequency MSI ( MSI - H ). |
| 0.5782 | Of 61 GCs investigated, 5 ( 8. 1 % ) tumors presented DNA_methylationhMLH1 methylation , 16 ( 26. 2 % ) and 25 ( 40. 9 % ) showed E - cadherin and p16 methylation respectively, and 8 ( 13. 1 % ) presented high - frequency MSI ( MSI - H ). |
| Score | Text |
|---|---|
| 0.9989 | Of the 8 MSI - H patients, 5 presented ProteinhMLH1 methylation, whereas no low - frequency MSI ( MSI - L ) and microsatellite stable ( MSS ) cases exhibited hMLH1 methylation ( 5 / 8 vs. 0 / 43, p < 0. 00001 ). |
| 0.9979 | Of the 8 MSI - H patients, 5 presented hMLH1 methylation, whereas no low - frequency MSI ( MSI - L ) and microsatellite stable ( MSS ) cases exhibited ProteinhMLH1 methylation ( 5 / 8 vs. 0 / 43, p < 0. 00001 ). |
| 0.9875 | Of the 8 MSI - H patients, 5 presented hMLH1 methylation, whereas no low - frequency MSI ( MSI - L ) and microsatellite stable ( MSS ) cases exhibited hMLH1 DNA_methylationmethylation ( 5 / 8 vs. 0 / 43, p < 0. 00001 ). |
| 0.9875 | Of the 8 MSI - H patients, 5 presented hMLH1 DNA_methylationmethylation , whereas no low - frequency MSI ( MSI - L ) and microsatellite stable ( MSS ) cases exhibited hMLH1 methylation ( 5 / 8 vs. 0 / 43, p < 0. 00001 ). |
| Score | Text |
|---|---|
| 0.9964 | Furthermore, these patients also presented E - cadherin and Proteinp16 hypermethylation. |
| 0.9959 | Furthermore, these patients also presented ProteinE - cadherin and p16 hypermethylation. |
| 0.9495 | Furthermore, these patients also presented E - cadherin and p16 DNA_methylationhypermethylation . |
| Score | Text |
|---|---|
| 0.9966 | Our data showed a significant correlation between ProteinhMLH1 methylation and MSI in GC, and suggested that a common mechanism of aberrant de novo methylation can be postulated in these cancers. |
| 0.9558 | Our data showed a significant correlation between hMLH1 DNA_methylationmethylation and MSI in GC, and suggested that a common mechanism of aberrant de novo methylation can be postulated in these cancers. |
| Score | Text |
|---|---|
| 0.9781 | Effect of ProteinHSP47 on prolyl 4 - hydroxylation of collagen model peptides. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9991 | ProteinHSP47 is a collagen - binding stress protein which also resides in the endoplasmic reticulum ( Nagata, K. and Yamada, K. M. ( 1986 ) J. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9912 | Both prolyl 4 - hydroxylase and ProteinHSP47 interact with procollagen alpha - chains during their folding and / or modification in the endoplasmic reticulum. |
| Score | Text |
|---|---|
| 0.9815 | Recent study has revealed that a simple collagen model peptide, ( Pro - Pro - Gly ) n, is recognized by ProteinHSP47 as well as by prolyl 4 - hydroxylase in vitro ( Koide et al., manuscript submitted ). |
| Score | Text |
|---|---|
| 0.9723 | In the present study, we investigated the effect of ProteinHSP47 on the prolyl 4 - hydroxylation of such collagen model peptides. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9884 | When ProteinHSP47 was added to the reaction mixture, substrate and less - hydroxylated materials accumulated. |
| Score | Text |
|---|---|
| 0.9971 | This effect depended on the peptide - binding activity of HSP47, because a mutant ProteinHSP47 without collagen - binding activity did not show any inhibitory effect on prolyl 4 - hydroxylation. |
| 0.9959 | This effect depended on the peptide - binding activity of ProteinHSP47 , because a mutant HSP47 without collagen - binding activity did not show any inhibitory effect on prolyl 4 - hydroxylation. |
| Score | Text |
|---|---|
| 0.9830 | Kinetic analysis and other biochemical analyses suggest that ProteinHSP47 retards the enzymatic reaction competing for the substrate peptide. |
| Score | Text |
|---|---|
| 0.9999 | Mouse K - Cl cotransporter ProteinKCC1 : cloning, mapping, pathological expression, and functional regulation. |
| Score | Text |
|---|---|
| 0.9989 | Although K - Cl cotransporter ( KCC1 ) mRNA is expressed in many tissues, K - Cl cotransport activity has been measured in few cell types, and detection of endogenous ProteinKCC1 polypeptide has not yet been reported. |
| 0.9807 | Although K - Cl cotransporter Protein( KCC1 ) mRNA is expressed in many tissues, K - Cl cotransport activity has been measured in few cell types, and detection of endogenous KCC1 polypeptide has not yet been reported. |
| Score | Text |
|---|---|
| 0.9998 | We have cloned the mouse erythroid KCC1 ( mKCC1 ) cDNA and its flanking genomic regions and mapped the ProteinmKCC1 gene to chromosome 8. |
| 0.9816 | We have cloned the mouse erythroid KCC1 Protein( mKCC1 ) cDNA and its flanking genomic regions and mapped the mKCC1 gene to chromosome 8. |
| 0.9722 | We have cloned the mouse erythroid ProteinKCC1 ( mKCC1 ) cDNA and its flanking genomic regions and mapped the mKCC1 gene to chromosome 8. |
| 0.8525 | We have cloned the mouse erythroid ProteinKCC1 ( mKCC1 ) cDNA and its flanking genomic regions and mapped the mKCC1 gene to chromosome 8. |
| Score | Text |
|---|---|
| 0.9997 | Three anti - peptide antibodies raised against recombinant ProteinmKCC1 function as immunoblot and immunoprecipitation reagents. |
| Score | Text |
|---|---|
| 0.9997 | The tissue distributions of mKCC1 mRNA and protein are widespread, and ProteinmKCC1 RNA is constitutively expressed during erythroid differentiation of ES cells. |
| 0.9997 | The tissue distributions of ProteinmKCC1 mRNA and protein are widespread, and mKCC1 RNA is constitutively expressed during erythroid differentiation of ES cells. |
| Score | Text |
|---|---|
| 0.9997 | ProteinKCC1 polypeptide or related antigen is present in erythrocytes of multiple species in which K - Cl cotransport activity has been documented. |
| Score | Text |
|---|---|
| 0.9978 | Erythroid ProteinKCC1 polypeptide abundance is elevated in proportion to reticulocyte counts in density - fractionated cells, in bleeding - induced reticulocytosis, in mouse models of sickle cell disease and thalassemia, and in the corresponding human disorders. mKCC1 - mediated uptake of ( 86 ) Rb into Xenopus oocytes requires extracellular Cl ( - ), is blocked by the diuretic R ( + ) - [ 2 - n - butyl - 6, 7 - dichloro - 2 - cyclopentyl - 2, 3 - dihydro - 1 - oxo - 1H - indenyl - 5 - yl - ) oxy ] acetic acid, and exhibits an erythroid pattern of acute regulation, with activation by hypotonic swelling, N - ethylmaleimide, and staurosporine and inhibition by calyculin and okadaic acid. |
| 0.9933 | Erythroid KCC1 polypeptide abundance is elevated in proportion to reticulocyte counts in density - fractionated cells, in bleeding - induced reticulocytosis, in mouse models of sickle cell disease and thalassemia, and in the corresponding human disorders. ProteinmKCC1 - mediated uptake of ( 86 ) Rb into Xenopus oocytes requires extracellular Cl ( - ), is blocked by the diuretic R ( + ) - [ 2 - n - butyl - 6, 7 - dichloro - 2 - cyclopentyl - 2, 3 - dihydro - 1 - oxo - 1H - indenyl - 5 - yl - ) oxy ] acetic acid, and exhibits an erythroid pattern of acute regulation, with activation by hypotonic swelling, N - ethylmaleimide, and staurosporine and inhibition by calyculin and okadaic acid. |
| Score | Text |
|---|---|
| 0.9998 | These reagents and findings will expedite studies of ProteinKCC1 structure - function relationships and of the pathobiology of KCC1 - mediated K - Cl cotransport. |
| 0.9959 | These reagents and findings will expedite studies of KCC1 structure - function relationships and of the pathobiology of ProteinKCC1 - mediated K - Cl cotransport. |
| Score | Text |
|---|---|
| 0.8841 | Progesterone metabolism in the human kidney and inhibition of Protein11beta - hydroxysteroid dehydrogenase type 2 by progesterone and its metabolites. |
| Score | Text |
|---|---|
| 0.8592 | Progesterone binds with high affinity to the Proteinmineralocorticoid ( MC ) receptor , but confers only very low agonistic MC activity. |
| 0.6067 | Progesterone binds with high affinity to the mineralocorticoid Protein( MC ) receptor , but confers only very low agonistic MC activity. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| One explanation for this phenomenon could be local metabolism of progesterone in the human kidney, similar to the inactivation of cortisol to cortisone by the Protein11beta - hydroxysteroid dehydrogenase ( 11beta - HSD ) type 2 . | |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.8784 | Using human kidney cortex microsomes, we tested the inhibitory potency of progesterone and its metabolites on the Protein11beta - HSD type 2 . |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9603 | In addition to progesterone metabolism by the kidney, the inhibition of Protein11beta - HSD type 2 by progesterone and its metabolites could be a second explanation for the weak MC - antagonist activity of progesterone in vivo. |
| Score | Text |
|---|---|
| 0.9710 | Inhibition of Protein11beta - HSD type 2 leads to an increase of intracellular cortisol in a way that the local equilibrium between the MC agonist cortisol and the antagonist progesterone is shifted to the agonist side. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9611 | INTERVENTION ( S ) : We removed three glycosylation signals from an hCG - hFSH chimera known to have high affinity for LH and ProteinFSH receptors , expecting this would create a bifunctional antagonist ( dgCFC ). |
| 0.9513 | INTERVENTION ( S ) : We removed three glycosylation signals from an hCG - hFSH chimera known to have high affinity for ProteinLH and FSH receptors, expecting this would create a bifunctional antagonist ( dgCFC ). |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9893 | RESULT ( S ) : dgCFC bound LH or ProteinFSH receptors similar to hCG or hFSH. |
| 0.9818 | RESULT ( S ) : dgCFC bound ProteinLH or FSH receptors similar to hCG or hFSH. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9476 | Regulation of Proteinthyrotropin receptor protein expression in insect cells. |
| Score | Text |
|---|---|
| 0.9694 | Expression of large quantities of conformationally intact thyrotropin receptor Protein( TSHR ) is essential to understand the structure - function relationship of the receptor. |
| 0.9445 | Expression of large quantities of conformationally intact Proteinthyrotropin receptor ( TSHR ) is essential to understand the structure - function relationship of the receptor. |
| Score | Text |
|---|---|
| 0.9993 | We expressed three different constructs of full - length human ProteinTSHR in insect cells : ( a ) a TSHR cDNA lacking signal sequence ( TSHR - ns ), ( b ) a TSHR cDNA containing human TSHR signal sequence ( TSHR - hs ) and ( c ) a TSHR cDNA with baculovirus envelope protein encoded signal sequence gp - 67 ( TSHR - gp ). |
| 0.9984 | We expressed three different constructs of full - length human TSHR in insect cells : ( a ) a TSHR cDNA lacking signal sequence ( TSHR - ns ), ( b ) a TSHR cDNA containing human TSHR signal sequence ( TSHR - hs ) and ( c ) a ProteinTSHR cDNA with baculovirus envelope protein encoded signal sequence gp - 67 ( TSHR - gp ). |
| 0.9972 | We expressed three different constructs of full - length human TSHR in insect cells : ( a ) a ProteinTSHR cDNA lacking signal sequence ( TSHR - ns ), ( b ) a TSHR cDNA containing human TSHR signal sequence ( TSHR - hs ) and ( c ) a TSHR cDNA with baculovirus envelope protein encoded signal sequence gp - 67 ( TSHR - gp ). |
| 0.9963 | We expressed three different constructs of full - length human TSHR in insect cells : ( a ) a TSHR cDNA lacking signal sequence ( TSHR - ns ), ( b ) a TSHR cDNA containing human ProteinTSHR signal sequence ( TSHR - hs ) and ( c ) a TSHR cDNA with baculovirus envelope protein encoded signal sequence gp - 67 ( TSHR - gp ). |
| 0.9963 | We expressed three different constructs of full - length human TSHR in insect cells : ( a ) a TSHR cDNA lacking signal sequence ( TSHR - ns ), ( b ) a ProteinTSHR cDNA containing human TSHR signal sequence ( TSHR - hs ) and ( c ) a TSHR cDNA with baculovirus envelope protein encoded signal sequence gp - 67 ( TSHR - gp ). |
| 0.9937 | We expressed three different constructs of full - length human TSHR in insect cells : ( a ) a TSHR cDNA lacking signal sequence ( TSHR - ns ), ( b ) a TSHR cDNA containing human TSHR signal sequence Protein( TSHR - hs ) and ( c ) a TSHR cDNA with baculovirus envelope protein encoded signal sequence gp - 67 ( TSHR - gp ). |
| 0.9901 | We expressed three different constructs of full - length human TSHR in insect cells : ( a ) a TSHR cDNA lacking signal sequence Protein( TSHR - ns ) , ( b ) a TSHR cDNA containing human TSHR signal sequence ( TSHR - hs ) and ( c ) a TSHR cDNA with baculovirus envelope protein encoded signal sequence gp - 67 ( TSHR - gp ). |
| 0.9901 | We expressed three different constructs of full - length human TSHR in insect cells : ( a ) a TSHR cDNA lacking signal sequence ( TSHR - ns ), ( b ) a TSHR cDNA containing human TSHR signal sequence ( TSHR - hs ) and ( c ) a TSHR cDNA with baculovirus envelope protein encoded signal sequence gp - 67 Protein( TSHR - gp ) . |
| 0.7322 | We expressed three different constructs of full - length human TSHR in insect cells : ( a ) a TSHR cDNA lacking signal sequence ( TSHR - ns ), ( b ) a TSHR cDNA containing human TSHR signal sequence ( TSHR - hs ) and ( c ) a TSHR cDNA with baculovirus envelope protein encoded signal sequence Proteingp - 67 ( TSHR - gp ). |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9996 | However, Western blot using TSHR specific monoclonal antibody showed unique bands around 80, 100 and 100 kDa in TSHR - ns, ProteinTSHR - hs and TSHR - gp virus infected insect cells respectively. |
| 0.9996 | However, Western blot using TSHR specific monoclonal antibody showed unique bands around 80, 100 and 100 kDa in ProteinTSHR - ns , TSHR - hs and TSHR - gp virus infected insect cells respectively. |
| 0.9994 | However, Western blot using TSHR specific monoclonal antibody showed unique bands around 80, 100 and 100 kDa in TSHR - ns, TSHR - hs and ProteinTSHR - gp virus infected insect cells respectively. |
| 0.9989 | However, Western blot using ProteinTSHR specific monoclonal antibody showed unique bands around 80, 100 and 100 kDa in TSHR - ns, TSHR - hs and TSHR - gp virus infected insect cells respectively. |
| Score | Text |
|---|---|
| 0.9988 | All three full - length ProteinTSHR proteins could neutralize the TSH binding inhibitory immunoglobulin ( TBII ) activity from sera of experimental animals. |
| Score | Text |
|---|---|
| 0.9993 | However, only glycosylated proteins ( TSHR - hs and ProteinTSHR - gp ) neutralized the TBII activity of sera from autoimmune thyroid patients, confirming the importance of glycosylation for patient autoantibody reactivity. |
| 0.9981 | However, only glycosylated proteins Protein( TSHR - hs and TSHR - gp ) neutralized the TBII activity of sera from autoimmune thyroid patients, confirming the importance of glycosylation for patient autoantibody reactivity. |
| 0.9720 | However, only Glycosylationglycosylated proteins ( TSHR - hs and TSHR - gp ) neutralized the TBII activity of sera from autoimmune thyroid patients, confirming the importance of glycosylation for patient autoantibody reactivity. |
| 0.8409 | However, only glycosylated proteins ( TSHR - hs and TSHR - gp ) neutralized the TBII activity of sera from autoimmune thyroid patients, confirming the importance of Glycosylationglycosylation for patient autoantibody reactivity. |
| Score | Text |
|---|---|
| 0.9994 | Expression levels of full - length ProteinTSHR proteins were much lower than the levels of similarly produced corresponding ectodomains of TSHR proteins. |
| 0.9990 | Expression levels of full - length TSHR proteins were much lower than the levels of similarly produced corresponding ectodomains of ProteinTSHR proteins. |
| Score | Text |
|---|---|
| 0.9998 | Southern blot and Northern blot analyses showed that DNA and RNA levels in full - length TSHR virus infected insect cells were comparable to the levels found in cells infected with viruses encoding only the ectodomain of ProteinTSHR . |
| Score | Text |
|---|---|
| 0.9996 | These data suggest that full - length ProteinTSHR expression is very low and is regulated at the translational level. |
| Score | Text |
|---|---|
| 0.9996 | ProteinBasT , a membrane - bound transducer protein for amino acid detection in Halobacterium salinarum. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9996 | We show here that ProteinBasT is a halobacterial transducer protein ( Htp ) responsible for chemotaxis towards five attractant amino acids. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9996 | Hydropathy analysis predicts an enterobacterial - type transducer protein topology for ProteinBasT , with an extracellular putative ligand - binding domain flanked by two transmembrane helices and a cytoplasmic domain. |
| Score | Text |
|---|---|
| 0.9998 | ProteinBasT - inactivated mutant cells are missing a membrane protein radiolabelled with L - [ methyl - 3H ] - methionine in wild - type cells, confirming that BasT is methylatable and membrane bound. |
| 0.9986 | BasT - inactivated mutant cells are missing a membrane protein radiolabelled with L - [ methyl - 3H ] - methionine in wild - type cells, confirming that ProteinBasT is methylatable and membrane bound. |
| 0.8197 | BasT - inactivated mutant cells are missing a membrane protein radiolabelled with L - [ methyl - 3H ] - methionine in wild - type cells, confirming that BasT is Methylationmethylatable and membrane bound. |
| Score | Text |
|---|---|
| 0.9992 | Behavioural analysis of the ProteinbasT mutant cells by capillary and chemical - in - plug assays demonstrates complete loss of chemotactic responses towards five ( leucine, isoleucine, valine, methionine and cysteine ) of the six attractant amino acids for Halobacterium salinarum, whereas they still respond to arginine. |
| Score | Text |
|---|---|
| 0.9986 | The volatile methyl group production assays also corroborate these findings and confirm that ProteinBasT signalling induces methyl group turnover. |
| Score | Text |
|---|---|
| 0.9997 | Our data identify ProteinBasT as the chemotaxis transducer protein for the branched chain amino acids leucine, isoleucine and valine as well as for methionine and cysteine. |
| Score | Text |
|---|---|
| 0.9998 | Thus, ProteinBasT and the arginine sensor Car cover the entire spectrum of chemotactic responses towards attractant amino acids in H. salinarum. |
| 0.9991 | Thus, BasT and the arginine sensor ProteinCar cover the entire spectrum of chemotactic responses towards attractant amino acids in H. salinarum. |
| Score | Text |
|---|---|
| 0.9937 | Additional N - glycosylation at Asn ( 13 ) rescues the human ProteinLHbeta - subunit from disulfide - linked aggregation. |
| 0.9927 | Additional GlycosylationN - glycosylation at Asn ( 13 ) rescues the human LHbeta - subunit from disulfide - linked aggregation. |
| 0.9679 | Additional N - glycosylation at EntityAsn ( 13 ) rescues the human LHbeta - subunit from disulfide - linked aggregation. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9998 | Despite the considerable homology between LHbeta and CGbeta, we previously demonstrated that, when expressed in GH ( 3 ) cells, the secreted form of ProteinLHbeta showed mispaired disulfide - linked aggregation in addition to monomer, whereas no aggregation was observed in CGbeta. |
| 0.9998 | Despite the considerable homology between ProteinLHbeta and CGbeta, we previously demonstrated that, when expressed in GH ( 3 ) cells, the secreted form of LHbeta showed mispaired disulfide - linked aggregation in addition to monomer, whereas no aggregation was observed in CGbeta. |
| 0.9998 | Despite the considerable homology between LHbeta and ProteinCGbeta , we previously demonstrated that, when expressed in GH ( 3 ) cells, the secreted form of LHbeta showed mispaired disulfide - linked aggregation in addition to monomer, whereas no aggregation was observed in CGbeta. |
| 0.9997 | Despite the considerable homology between LHbeta and CGbeta, we previously demonstrated that, when expressed in GH ( 3 ) cells, the secreted form of LHbeta showed mispaired disulfide - linked aggregation in addition to monomer, whereas no aggregation was observed in ProteinCGbeta . |
| Score | Text |
|---|---|
| 0.9996 | To determine the domains which are associated with the ProteinLHbeta - aggregation and which prevent CGbeta - aggregation, mutant beta - subunits in glycosylation and carboxy - terminus were expressed in GH ( 3 ) cells, and the occurrence of aggregation was assessed by continuous labeling with [ 35S ] methionine / cysteine, immunoprecipitation with anti - hCGbeta serum, and sodium dodecyl sulfate - polyacrylamide gel electrophoresis in a non - reducing condition. |
| 0.9994 | To determine the domains which are associated with the LHbeta - aggregation and which prevent ProteinCGbeta - aggregation , mutant beta - subunits in glycosylation and carboxy - terminus were expressed in GH ( 3 ) cells, and the occurrence of aggregation was assessed by continuous labeling with [ 35S ] methionine / cysteine, immunoprecipitation with anti - hCGbeta serum, and sodium dodecyl sulfate - polyacrylamide gel electrophoresis in a non - reducing condition. |
| 0.9960 | To determine the domains which are associated with the LHbeta - aggregation and which prevent CGbeta - aggregation, mutant beta - subunits in glycosylation and carboxy - terminus were expressed in GH ( 3 ) cells, and the occurrence of aggregation was assessed by continuous labeling with [ 35S ] methionine / cysteine, immunoprecipitation with Proteinanti - hCGbeta serum, and sodium dodecyl sulfate - polyacrylamide gel electrophoresis in a non - reducing condition. |
| 0.5586 | To determine the domains which are associated with the LHbeta - aggregation and which prevent CGbeta - aggregation, mutant beta - subunits in Glycosylationglycosylation and carboxy - terminus were expressed in GH ( 3 ) cells, and the occurrence of aggregation was assessed by continuous labeling with [ 35S ] methionine / cysteine, immunoprecipitation with anti - hCGbeta serum, and sodium dodecyl sulfate - polyacrylamide gel electrophoresis in a non - reducing condition. |
| Score | Text |
|---|---|
| 0.9873 | No aggregation was seen when N - linked oligosaccharides were attached to the Asn ( 13 ) of ProteinLHbeta . |
| 0.9754 | No aggregation was seen when N - linked oligosaccharides were attached to the EntityAsn ( 13 ) of LHbeta. |
| 0.9257 | No aggregation was seen when N - linked Entityoligosaccharides were attached to the Asn ( 13 ) of LHbeta. |
| 0.6661 | No aggregation was seen when N - linked oligosaccharides were Glycosylationattached to the Asn ( 13 ) of LHbeta. |
| Score | Text |
|---|---|
| 0.9914 | Removal of the carbohydrate unit at the EntityAsn ( 13 ) of CGbeta caused aggregation, although the amount was less than 10 % of monomer. |
| 0.9859 | Removal of the carbohydrate unit at the Asn ( 13 ) of ProteinCGbeta caused aggregation, although the amount was less than 10 % of monomer. |
| 0.8673 | Removal of the Entitycarbohydrate unit at the Asn ( 13 ) of CGbeta caused aggregation, although the amount was less than 10 % of monomer. |
| 0.4781 | DeglycosylationRemoval of the carbohydrate unit at the Asn ( 13 ) of CGbeta caused aggregation, although the amount was less than 10 % of monomer. |
| 0.8217 | Removal of the Entitycarbohydrate unit at the Asn ( 13 ) of CGbeta caused aggregation, although the amount was less than 10 % of monomer. |
| Score | Text |
|---|---|
| 0.9987 | The carboxy - terminal regions of neither LHbeta nor ProteinCGbeta were associated with their aggregation. |
| 0.9982 | The carboxy - terminal regions of neither ProteinLHbeta nor CGbeta were associated with their aggregation. |
| Score | Text |
|---|---|
| 0.9988 | Both CGbeta wild - type ( WT ) and ProteinCGbeta lacking N - glycosylation at Asn ( 13 ) ( CGbeta - N13 ) showed aggregates in lysate. |
| 0.9969 | Both ProteinCGbeta wild - type ( WT ) and CGbeta lacking N - glycosylation at Asn ( 13 ) ( CGbeta - N13 ) showed aggregates in lysate. |
| 0.9872 | Both CGbeta wild - type ( WT ) and CGbeta lacking GlycosylationN - glycosylation at Asn ( 13 ) ( CGbeta - N13 ) showed aggregates in lysate. |
| 0.9241 | Both CGbeta wild - type ( WT ) and CGbeta lacking N - glycosylation at EntityAsn ( 13 ) ( CGbeta - N13 ) showed aggregates in lysate. |
| Score | Text |
|---|---|
| 0.9992 | However, in contrast to CGbeta - N13, ProteinCGbetaWT revealed no aggregation in medium. |
| 0.9984 | However, in contrast to ProteinCGbeta - N13 , CGbetaWT revealed no aggregation in medium. |
| Score | Text |
|---|---|
| 0.9966 | These results indicate that the backbone structure consisting of 114 amino acids and N - linked glycosylation at Asn ( 30 ) is involved in the aggregation of ProteinLHbeta . |
| 0.9745 | These results indicate that the backbone structure consisting of 114 amino acids and N - linked glycosylation at EntityAsn ( 30 ) is involved in the aggregation of LHbeta. |
| 0.8888 | These results indicate that the backbone structure consisting of 114 amino acids and GlycosylationN - linked glycosylation at Asn ( 30 ) is involved in the aggregation of LHbeta. |
| 0.9807 | These results indicate that the backbone structure consisting of 114 amino acids and N - linked Glycosylationglycosylation at Asn ( 30 ) is involved in the aggregation of LHbeta. |
| Score | Text |
|---|---|
| 0.9965 | Moreover, N - glycosylation at Asn ( 13 ) does not prevent such aggregation, but instead plays an important role in correct folding for both ProteinLHbeta - and CGbeta - subunits to be secreted as monomer. |
| 0.9960 | Moreover, N - glycosylation at Asn ( 13 ) does not prevent such aggregation, but instead plays an important role in correct folding for both LHbeta - and ProteinCGbeta - subunits to be secreted as monomer. |
| 0.9920 | Moreover, GlycosylationN - glycosylation at Asn ( 13 ) does not prevent such aggregation, but instead plays an important role in correct folding for both LHbeta - and CGbeta - subunits to be secreted as monomer. |
| 0.9863 | Moreover, N - glycosylation at EntityAsn ( 13 ) does not prevent such aggregation, but instead plays an important role in correct folding for both LHbeta - and CGbeta - subunits to be secreted as monomer. |
| Score | Text |
|---|---|
| 0.9499 | ProteinType XIII collagen forms homotrimers with three triple helical collagenous domains and its association into disulfide - bonded trimers is enhanced by prolyl 4 - hydroxylase. |
| Score | Text |
|---|---|
| 0.9699 | ProteinType XIII collagen is a type II transmembrane protein predicted to consist of a short cytosolic domain, a single transmembrane domain, and three collagenous domains flanked by noncollagenous sequences. |
| 0.6768 | Type ProteinXIII collagen is a type II transmembrane protein predicted to consist of a short cytosolic domain, a single transmembrane domain, and three collagenous domains flanked by noncollagenous sequences. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9431 | In order to extend studies of Proteintype XIII collagen from cDNAs to the protein level we have produced it in insect cells by means of baculoviruses. |
| 0.5934 | In order to extend studies of type ProteinXIII collagen from cDNAs to the protein level we have produced it in insect cells by means of baculoviruses. |
| Score | Text |
|---|---|
| 0.9727 | Type XIII collagen alpha chains were found to associate into disulfide - bonded trimers, and Hydroxylationhydroxylation of proline residues dramatically enhanced this association. |
| 0.9044 | Type XIII collagen alpha chains were found to associate into disulfide - bonded trimers, and hydroxylation of Entityproline residues dramatically enhanced this association. |
| 0.7708 | ProteinType XIII collagen alpha chains were found to associate into disulfide - bonded trimers, and hydroxylation of proline residues dramatically enhanced this association. |
| 0.7303 | Type XIII collagen alpha chains were found to associate into disulfide - bonded trimers, and hydroxylation of Entityproline residues dramatically enhanced this association. |
| 0.6210 | ProteinType XIII collagen alpha chains were found to associate into disulfide - bonded trimers, and hydroxylation of proline residues dramatically enhanced this association. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9968 | ProteinPepsin and trypsin / chymotrypsin digestions indicated that the type XIII collagen alpha chains form homotrimers whose three collagenous domains are in triple helical conformation. |
| 0.7930 | Pepsin and trypsin / chymotrypsin digestions indicated that the Proteintype XIII collagen alpha chains form homotrimers whose three collagenous domains are in triple helical conformation. |
| 0.6860 | Pepsin and trypsin / chymotrypsin digestions indicated that the Proteintype XIII collagen alpha chains form homotrimers whose three collagenous domains are in triple helical conformation. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9342 | All in all, most of the Proteintype XIII collagen ectodomain appears to be present in triple helical conformation, which is in clear contrast to the short or highly interrupted triple helical domains of the other known collagenous transmembrane proteins. |
| Score | Text |
|---|---|
| 0.9804 | Symmetric and asymmetric DNA methylation in the human ProteinIGF2 - H19 imprinted region. |
| 0.8721 | Symmetric and asymmetric DNA_methylationDNA methylation in the human IGF2 - H19 imprinted region. |
| 0.7417 | Symmetric and asymmetric DNA methylation in the human IGF2 - H19 Entityimprinted region . |
| 0.9222 | Symmetric and asymmetric DNA DNA_methylationmethylation in the human IGF2 - H19 imprinted region. |
| 0.6758 | Symmetric and asymmetric DNA_methylationDNA methylation in the human IGF2 - H19 imprinted region. |
| 0.6149 | Symmetric and asymmetric DNA methylation in the human IGF2 - H19 Entityimprinted region. |
| Score | Text |
|---|---|
| 0.9989 | The two contiguous IGF2 ( human insulin - like growth factor II ) and ProteinH19 genes are reciprocally imprinted in both human and mouse. |
| 0.9986 | The two contiguous ProteinIGF2 ( human insulin - like growth factor II ) and H19 genes are reciprocally imprinted in both human and mouse. |
| 0.8282 | The two contiguous IGF2 ( human Proteininsulin - like growth factor II ) and H19 genes are reciprocally imprinted in both human and mouse. |
| Score | Text |
|---|---|
| 0.9996 | In most tissues, IGF2 is transcribed only from the paternal chromosome while ProteinH19 is transcribed only from the maternal allele. |
| 0.9996 | In most tissues, ProteinIGF2 is transcribed only from the paternal chromosome while H19 is transcribed only from the maternal allele. |
| Score | Text |
|---|---|
| 0.9881 | The presence of a differential methylation region ( DMR ) on the two parental alleles at the 5'flanking region of ProteinH19 has been proposed to constitute the gametic imprint, which controls the reciprocal allelic expression of the two genes. |
| 0.9682 | The presence of a differential DNA_methylationmethylation region ( DMR ) on the two parental alleles at the 5'flanking region of H19 has been proposed to constitute the gametic imprint, which controls the reciprocal allelic expression of the two genes. |
| 0.8126 | The presence of a differential methylation region ( DMR ) on the two parental alleles at the Entity5'flanking region of H19 has been proposed to constitute the gametic imprint, which controls the reciprocal allelic expression of the two genes. |
| 0.8506 | The presence of a differential methylation region ( DMR ) on the two parental alleles at the Entity5 ' flanking region of H19 has been proposed to constitute the gametic imprint, which controls the reciprocal allelic expression of the two genes. |
| 0.8239 | The presence of a differential methylation region ( DMR ) on the two parental alleles at the Entity5'flanking region of H19 has been proposed to constitute the gametic imprint, which controls the reciprocal allelic expression of the two genes. |
| 0.5867 | The presence of a differential methylation region ( DMR ) on the two parental alleles at the 5 ' Entityflanking region of H19 has been proposed to constitute the gametic imprint, which controls the reciprocal allelic expression of the two genes. |
| 0.5195 | The presence of a differential methylation region ( DMR ) on the two parental alleles at the 5 ' Entityflanking region of H19 has been proposed to constitute the gametic imprint, which controls the reciprocal allelic expression of the two genes. |
| Score | Text |
|---|---|
| 0.9914 | Using bisulfite genomic sequencing, we have assessed the methylation status of cytosine ( including 154 CpG sites ) in six CpG - rich regions of the human ProteinIGF2 - H19 genes. |
| 0.9168 | Using bisulfite genomic sequencing, we have assessed the methylation status of Entitycytosine ( including 154 CpG sites ) in six CpG - rich regions of the human IGF2 - H19 genes. |
| 0.9051 | Using bisulfite genomic sequencing, we have assessed the DNA_methylationmethylation status of cytosine ( including 154 CpG sites ) in six CpG - rich regions of the human IGF2 - H19 genes. |
| Score | Text |
|---|---|
| 0.9990 | In a CpG island near promoter P3 of the ProteinIGF2 gene, more than 99. 8 % of all cytosines were converted to thymidine by sodium bisulfite mutagenesis, indicating that none of the CpGs was methylated. |
| 0.9128 | In a CpG island near promoter P3 of the IGF2 gene, more than 99. 8 % of all cytosines were converted to thymidine by sodium bisulfite mutagenesis, indicating that none of the CpGs was DNA_methylationmethylated . |
| 0.6624 | In a EntityCpG island near promoter P3 of the IGF2 gene, more than 99. 8 % of all cytosines were converted to thymidine by sodium bisulfite mutagenesis, indicating that none of the CpGs was methylated. |
| 0.8559 | In a CpG island near promoter P3 of the IGF2 gene, more than 99. 8 % of all Entitycytosines were converted to thymidine by sodium bisulfite mutagenesis, indicating that none of the CpGs was methylated. |
| 0.5444 | In a CpG island near promoter P3 of the IGF2 gene, more than 99. 8 % of all cytosines were converted to thymidine by sodium bisulfite mutagenesis, indicating that none of the EntityCpGs was methylated. |
| Score | Text |
|---|---|
| 0.9955 | In the ProteinIGF2 exon 8 - 9 region, mosaic methylation of 56 CpG sites was observed in fetal tissues and in adult blood DNA. |
| 0.9840 | In the IGF2 exon 8 - 9 region, mosaic DNA_methylationmethylation of 56 CpG sites was observed in fetal tissues and in adult blood DNA. |
| 0.6755 | In the IGF2 exon 8 - 9 region, mosaic methylation of 56 EntityCpG sites was observed in fetal tissues and in adult blood DNA. |
| 0.5131 | In the IGF2 exon 8 - 9 region, mosaic methylation of 56 EntityCpG sites was observed in fetal tissues and in adult blood DNA. |
| Score | Text |
|---|---|
| 0.9983 | In contrast to the mosaic methylation of ProteinIGF2 , the allelic methylation of the human H19 DMR was uniform. |
| 0.9495 | In contrast to the mosaic methylation of IGF2, the allelic DNA_methylationmethylation of the human H19 DMR was uniform. |
| 0.9479 | In contrast to the mosaic methylation of IGF2, the allelic methylation of the human ProteinH19 DMR was uniform. |
| 0.9345 | In contrast to the mosaic DNA_methylationmethylation of IGF2, the allelic methylation of the human H19 DMR was uniform. |
| 0.8976 | In contrast to the mosaic methylation of IGF2, the allelic methylation of the human H19 EntityDMR was uniform. |
| Score | Text |
|---|---|
| 0.9967 | In the CpG region located 2 kb upstream ( - 2362 to - 1911 ) of the ProteinH19 transcription site, all 25 CpG sites were completely methylated on only one parental allele. |
| 0.9885 | In the CpG region located 2 kb upstream ( - 2362 to - 1911 ) of the H19 transcription site, all 25 CpG sites were completely DNA_methylationmethylated on only one parental allele. |
| 0.8887 | In the CpG region located 2 kb upstream ( - 2362 to - 1911 ) of the H19 transcription site, all Entity25 CpG sites were completely methylated on only one parental allele. |
| 0.9163 | In the CpG region located 2 kb upstream ( - 2362 to - 1911 ) of the H19 transcription site, all 25 EntityCpG sites were completely methylated on only one parental allele. |
| 0.5610 | In the CpG region located 2 kb upstream ( - 2362 to - 1911 ) of the H19 transcription site, all Entity25 CpG sites were completely methylated on only one parental allele. |
| 0.5387 | In the CpG region located 2 kb upstream ( - 2362 to - 1911 ) of the H19 transcription site, all 25 EntityCpG sites were completely methylated on only one parental allele. |
| 0.5386 | In the CpG region located 2 kb upstream ( - 2362 to - 1911 ) of the H19 transcription site, all Entity25 CpG sites were completely methylated on only one parental allele. |
| Score | Text |
|---|---|
| 0.9920 | Uniform allele - specific DNA_methylationmethylation was also observed in the CpG island proximal to the H19 promoter ( - 711 to - 290 ) with complete methylation of all 25 CpG sites in one parental allele. |
| 0.9834 | Uniform allele - specific methylation was also observed in the CpG island proximal to the H19 promoter ( - 711 to - 290 ) with complete DNA_methylationmethylation of all 25 CpG sites in one parental allele. |
| 0.9734 | Uniform allele - specific methylation was also observed in the CpG island proximal to the ProteinH19 promoter ( - 711 to - 290 ) with complete methylation of all 25 CpG sites in one parental allele. |
| 0.6477 | Uniform allele - specific methylation was also observed in the EntityCpG island proximal to the H19 promoter ( - 711 to - 290 ) with complete methylation of all 25 CpG sites in one parental allele. |
| 0.7181 | Uniform allele - specific methylation was also observed in the CpG island proximal to the H19 promoter ( - 711 to - 290 ) with complete methylation of all 25 EntityCpG sites in one parental allele. |
| 0.5004 | Uniform allele - specific methylation was also observed in the CpG island proximal to the H19 promoter ( - 711 to - 290 ) with DNA_methylationcomplete methylation of all 25 CpG sites in one parental allele. |
| Uniform allele - specific methylation was also observed in the CpG island proximal to the H19 promoter ( - 711 to - 290 ) with complete methylation of all Entity25 CpG sites in one parental allele. | |
| Score | Text |
|---|---|
| 0.9850 | In contrast, the CpG region in the H19 promoter ( - 292 to + 15 ) was mosaically DNA_methylationmethylated in all tissues. |
| 0.9604 | In contrast, the CpG region in the ProteinH19 promoter ( - 292 to + 15 ) was mosaically methylated in all tissues. |
| 0.8898 | In contrast, the EntityCpG region in the H19 promoter ( - 292 to + 15 ) was mosaically methylated in all tissues. |
| 0.7647 | In contrast, the EntityCpG region in the H19 promoter ( - 292 to + 15 ) was mosaically methylated in all tissues. |
| Score | Text |
|---|---|
| 0.9719 | In addition, cytosine was DNA_methylationmethylated at three CpNpG and GpNpC sites on the top DNA strand and one CpNpG site on the bottom DNA strand from the fetal brain. |
| 0.9107 | In addition, cytosine was methylated at three EntityCpNpG and GpNpC sites on the top DNA strand and one CpNpG site on the bottom DNA strand from the fetal brain. |
| 0.9007 | In addition, cytosine was methylated at three CpNpG and EntityGpNpC sites on the top DNA strand and one CpNpG site on the bottom DNA strand from the fetal brain. |
| 0.8889 | In addition, cytosine was methylated at three CpNpG and GpNpC sites on the top DNA strand and one EntityCpNpG site on the bottom DNA strand from the fetal brain. |
| Score | Text |
|---|---|
| 0.9566 | The cytosines at CpG sites were methylated on both DNA strands ( symmetric methylation ) while cytosines at the CpNpG and GpNpC sites were DNA_methylationmethylated on only one DNA strand ( asymmetric methylation ). |
| 0.9546 | The cytosines at CpG sites were DNA_methylationmethylated on both DNA strands ( symmetric methylation ) while cytosines at the CpNpG and GpNpC sites were methylated on only one DNA strand ( asymmetric methylation ). |
| 0.9444 | The cytosines at CpG sites were methylated on both DNA strands ( symmetric methylation ) while Entitycytosines at the CpNpG and GpNpC sites were methylated on only one DNA strand ( asymmetric methylation ). |
| 0.9244 | The Entitycytosines at CpG sites were methylated on both DNA strands ( symmetric methylation ) while cytosines at the CpNpG and GpNpC sites were methylated on only one DNA strand ( asymmetric methylation ). |
| Score | Text |
|---|---|
| 0.9931 | The asymmetric methylation was associated with tissue - specific disruption of ProteinH19 genomic imprinting in fetal brain. |
| 0.9505 | The asymmetric DNA_methylationmethylation was associated with tissue - specific disruption of H19 genomic imprinting in fetal brain. |
| Score | Text |
|---|---|
| 0.9982 | An increase in histone acetylation and ProteinIL - 2 antagonizing the immunoinhibitory effect are necessary for augmentation by butyrate of in vitro anti - TNP antibody production. |
| 0.9969 | An increase in histone Acetylationacetylation and IL - 2 antagonizing the immunoinhibitory effect are necessary for augmentation by butyrate of in vitro anti - TNP antibody production. |
| 0.9952 | An increase in Proteinhistone acetylation and IL - 2 antagonizing the immunoinhibitory effect are necessary for augmentation by butyrate of in vitro anti - TNP antibody production. |
| Score | Text |
|---|---|
| 0.9977 | We investigated the role of Proteinhistone acetylation in the promotion of antigen - specific antibody production in murine B cells induced by sodium butyrate ( NaBu ) plus interleukin 2 ( IL - 2 ). |
| 0.9954 | We investigated the role of histone Acetylationacetylation in the promotion of antigen - specific antibody production in murine B cells induced by sodium butyrate ( NaBu ) plus interleukin 2 ( IL - 2 ). |
| 0.9559 | We investigated the role of histone acetylation in the promotion of antigen - specific antibody production in murine B cells induced by sodium butyrate ( NaBu ) plus interleukin 2 Protein( IL - 2 ) . |
| 0.8633 | We investigated the role of histone acetylation in the promotion of antigen - specific antibody production in murine B cells induced by sodium butyrate ( NaBu ) plus Proteininterleukin 2 ( IL - 2 ). |
| Score | Text |
|---|---|
| 0.9978 | NaBu dose dependently increased the acetylation levels of histone H4 at concentrations which effectively enhanced anti - trinitrophenyl ( TNP ) antibody production in the presence of ProteinIL - 2 . |
| 0.9956 | NaBu dose dependently increased the Acetylationacetylation levels of histone H4 at concentrations which effectively enhanced anti - trinitrophenyl ( TNP ) antibody production in the presence of IL - 2. |
| 0.9652 | NaBu dose dependently increased the acetylation levels of Proteinhistone H4 at concentrations which effectively enhanced anti - trinitrophenyl ( TNP ) antibody production in the presence of IL - 2. |
| Score | Text |
|---|---|
| 0.9955 | Among other short - chain fatty acids and NaBu analogs, propionate, valerate and vinylacetate were effective in the presence of ProteinIL - 2 in increasing both antibody production and the histone H4 acetylation level, but acetate, alpha -, beta - and gamma - hydroxybutyrates and alpha -, beta - and gamma - aminobutyrates were not effective, even in the presence of IL - 2. |
| 0.9955 | Among other short - chain fatty acids and NaBu analogs, propionate, valerate and vinylacetate were effective in the presence of IL - 2 in increasing both antibody production and the histone H4 acetylation level, but acetate, alpha -, beta - and gamma - hydroxybutyrates and alpha -, beta - and gamma - aminobutyrates were not effective, even in the presence of ProteinIL - 2 . |
| 0.9899 | Among other short - chain fatty acids and NaBu analogs, propionate, valerate and vinylacetate were effective in the presence of IL - 2 in increasing both antibody production and the histone H4 Acetylationacetylation level, but acetate, alpha -, beta - and gamma - hydroxybutyrates and alpha -, beta - and gamma - aminobutyrates were not effective, even in the presence of IL - 2. |
| 0.9753 | Among other short - chain fatty acids and NaBu analogs, propionate, valerate and vinylacetate were effective in the presence of IL - 2 in increasing both antibody production and the Proteinhistone H4 acetylation level, but acetate, alpha -, beta - and gamma - hydroxybutyrates and alpha -, beta - and gamma - aminobutyrates were not effective, even in the presence of IL - 2. |
| Score | Text |
|---|---|
| 0.9988 | The effect of the specific histone deacetylase inhibitor trichostatin A ( TSA ), which enhances anti - TNP antibody production without ProteinIL - 2 , was markedly inhibited by adding NaBu simultaneously. |
| 0.9979 | The effect of the specific Proteinhistone deacetylase inhibitor trichostatin A ( TSA ), which enhances anti - TNP antibody production without IL - 2, was markedly inhibited by adding NaBu simultaneously. |
| Score | Text |
|---|---|
| 0.9977 | However, the effect of TSA was neither inhibited nor potentiated by NaBu in the presence of ProteinIL - 2 . |
| Score | Text |
|---|---|
| 0.9962 | Splenic B cells treated with NaBu, TSA and both together in the presence or absence of IL - 2 showed almost the same increased Acetylationacetylation level of histone H4. |
| 0.9855 | Splenic B cells treated with NaBu, TSA and both together in the presence or absence of ProteinIL - 2 showed almost the same increased acetylation level of histone H4. |
| 0.9659 | Splenic B cells treated with NaBu, TSA and both together in the presence or absence of IL - 2 showed almost the same increased acetylation level of Proteinhistone H4 . |
| Score | Text |
|---|---|
| 0.9997 | These results suggest that the NaBu - induced enhancement of anti - TNP antibody production in the presence of IL - 2 is mediated through a moderate increase in the level of histone acetylation and that NaBu has both stimulating and inhibiting activities for anti - TNP antibody production, the latter of which is overcome by ProteinIL - 2 . |
| 0.9987 | These results suggest that the NaBu - induced enhancement of anti - TNP antibody production in the presence of ProteinIL - 2 is mediated through a moderate increase in the level of histone acetylation and that NaBu has both stimulating and inhibiting activities for anti - TNP antibody production, the latter of which is overcome by IL - 2. |
| 0.9973 | These results suggest that the NaBu - induced enhancement of anti - TNP antibody production in the presence of IL - 2 is mediated through a moderate increase in the level of histone Acetylationacetylation and that NaBu has both stimulating and inhibiting activities for anti - TNP antibody production, the latter of which is overcome by IL - 2. |
| 0.9956 | These results suggest that the NaBu - induced enhancement of anti - TNP antibody production in the presence of IL - 2 is mediated through a moderate increase in the level of Proteinhistone acetylation and that NaBu has both stimulating and inhibiting activities for anti - TNP antibody production, the latter of which is overcome by IL - 2. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9952 | To provide more reliable IFAs, we established recombinant Semliki Forest viruses ( rSFVs ) expressing the HHV - 8 - specific proteins ProteinORF73 and K8. 1 and used BHK - 21 cells infected with these rSFVs for IFA ( ORF73 - IFA and K8. 1 - IFA ). |
| 0.9944 | To provide more reliable IFAs, we established recombinant Semliki Forest viruses ( rSFVs ) expressing the HHV - 8 - specific proteins ORF73 and K8. 1 and used BHK - 21 cells infected with these rSFVs for IFA Protein( ORF73 - IFA and K8. 1 - IFA ). |
| 0.9680 | To provide more reliable IFAs, we established recombinant Semliki Forest viruses ( rSFVs ) expressing the HHV - 8 - specific proteins ORF73 and ProteinK8. 1 and used BHK - 21 cells infected with these rSFVs for IFA ( ORF73 - IFA and K8. 1 - IFA ). |
| 0.8660 | To provide more reliable IFAs, we established recombinant Semliki Forest viruses ( rSFVs ) expressing the HHV - 8 - specific proteins ORF73 and K8. 1 and used BHK - 21 cells infected with these rSFVs for IFA ( ORF73 - IFA and ProteinK8. 1 - IFA ) . |
| 0.8664 | To provide more reliable IFAs, we established recombinant Semliki Forest viruses ( rSFVs ) expressing the HHV - 8 - specific proteins ORF73 and K8. 1 and used BHK - 21 cells infected with these rSFVs for IFA ( ORF73 - IFA and K8 Protein. 1 - IFA ) . |
| 0.8454 | To provide more reliable IFAs, we established recombinant Semliki Forest viruses ( rSFVs ) expressing the HHV - 8 - specific proteins ORF73 and K8 Protein. 1 and used BHK - 21 cells infected with these rSFVs for IFA ( ORF73 - IFA and K8. 1 - IFA ). |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.8599 | The rSFV system also allowed detection of antibodies against glycosylation - dependent epitopes of ProteinK8. 1 . |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9991 | K8. 1 - IFA was more sensitive than either ProteinORF73 - IFA or peptide ELISAs. |
| Score | Text |
|---|---|
| 0.9467 | Using PEL - based lytic IFA as a reference assay, the sensitivity and specificity of ProteinK8. 1 - IFA were estimated to be 94 and 100 %, respectively. |
| 0.8804 | Using PEL - based lytic IFA as a reference assay, the sensitivity and specificity of K8 Protein. 1 - IFA were estimated to be 94 and 100 %, respectively. |
| Score | Text |
|---|---|
| 0.9696 | HHV - 8 prevalences determined by ProteinK8. 1 - IFA among the human immunodeficiency virus ( HIV ) - positive ( HIV ( + ) ) Kaposi's sarcoma ( KS ) patients, HIV ( + ) KS ( - ) patients, and healthy controls were 100, 65, and 6. 7 %, respectively, which were consistent with prior reports. |
| 0.9475 | HHV - 8 prevalences determined by K8 Protein. 1 - IFA among the human immunodeficiency virus ( HIV ) - positive ( HIV ( + ) ) Kaposi's sarcoma ( KS ) patients, HIV ( + ) KS ( - ) patients, and healthy controls were 100, 65, and 6. 7 %, respectively, which were consistent with prior reports. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9937 | Evidence that the lizard Proteinhelospectin peptides are O - glycosylated. |
| 0.9909 | Evidence that the lizard helospectin peptides are GlycosylationO - glycosylated . |
| Score | Text |
|---|---|
| 0.9973 | Six forms of Proteinhelospectin ( a vasoactive intestinal peptide analogue ) were purified from the venom of the Heloderma horridum lizard. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9993 | Two forms were identified as the previously named ProteinHs1 and Hs2 of 38 and 37 amino - acid residues, respectively. |
| 0.9988 | Two forms were identified as the previously named Hs1 and ProteinHs2 of 38 and 37 amino - acid residues, respectively. |
| Score | Text |
|---|---|
| 0.9626 | Two forms corresponded to Hs1 and Hs2 O - glycosylated by a N - acetylhexosamine - hexose motif attached to the EntitySer32 residue. |
| 0.9589 | Two forms corresponded to ProteinHs1 and Hs2 O - glycosylated by a N - acetylhexosamine - hexose motif attached to the Ser32 residue. |
| 0.9497 | Two forms corresponded to Hs1 and Hs2 O - glycosylated by a EntityN - acetylhexosamine - hexose motif attached to the Ser32 residue. |
| 0.9493 | Two forms corresponded to Hs1 and Hs2 GlycosylationO - glycosylated by a N - acetylhexosamine - hexose motif attached to the Ser32 residue. |
| 0.9234 | Two forms corresponded to Hs1 and ProteinHs2 O - glycosylated by a N - acetylhexosamine - hexose motif attached to the Ser32 residue. |
| 0.6560 | Two forms corresponded to Hs1 and GlycosylationHs2 O - glycosylated by a N - acetylhexosamine - hexose motif attached to the Ser32 residue. |
| Score | Text |
|---|---|
| 0.8040 | Two other forms were not completely characterized but might correspond to the GlycosylationO - glycosylated forms bearing a phosphate or a sulfate group. |
| Score | Text |
|---|---|
| 0.9992 | The glycosylation did not affect the capacity of the helospectins to recognize and to activate the human and the rat ProteinVPAC1 and VPAC2 receptors. |
| 0.9992 | The glycosylation did not affect the capacity of the helospectins to recognize and to activate the human and the rat VPAC1 and ProteinVPAC2 receptors. |
| 0.9919 | The glycosylation did not affect the capacity of the Proteinhelospectins to recognize and to activate the human and the rat VPAC1 and VPAC2 receptors. |
| 0.9814 | The Glycosylationglycosylation did not affect the capacity of the helospectins to recognize and to activate the human and the rat VPAC1 and VPAC2 receptors. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9985 | Liver - specific and non - liver - specific methionine adenosyltransferase ( MAT ) are products of two genes, MAT1A and ProteinMAT2A , respectively, that catalyze the formation of S - adenosylmethionine ( SAM ). |
| 0.9983 | Liver - specific and non - liver - specific methionine adenosyltransferase ( MAT ) are products of two genes, ProteinMAT1A and MAT2A, respectively, that catalyze the formation of S - adenosylmethionine ( SAM ). |
| Score | Text |
|---|---|
| 0.9971 | We previously showed that ProteinMAT2A expression was associated with more rapid cell growth. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9981 | After rats were fed intragastrically with ethanol and high fat for 9 wk, the mRNA level of both MAT forms doubled but only the protein level of ProteinMAT2A increased. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9997 | Hepatic levels of methionine, SAM, and DNA methylation fell by approximately 40 %. Proteinc - myc was hypomethylated, and its mRNA level increased. |
| 0.9195 | Hepatic levels of methionine, SAM, and DNA methylation fell by approximately 40 %. c - myc was DNA_methylationhypomethylated , and its mRNA level increased. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9998 | Thus in the prefibrotic stage of alcoholic liver injury, there is already a switch in MAT expression, global DNA hypomethylation, increased Proteinc - myc expression, and genome - wide DNA strand break. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9994 | Hsl7p, the yeast homologue of human ProteinJBP1 , is a protein methyltransferase. |
| 0.9994 | ProteinHsl7p , the yeast homologue of human JBP1, is a protein methyltransferase. |
| Score | Text |
|---|---|
| 0.9996 | The yeast protein ProteinHsl7p is a homologue of Janus kinase binding protein 1, JBP1, a newly characterized protein methyltransferase. |
| 0.9993 | The yeast protein Hsl7p is a homologue of Janus kinase binding protein 1, ProteinJBP1 , a newly characterized protein methyltransferase. |
| 0.7987 | The yeast protein Hsl7p is a homologue of ProteinJanus kinase binding protein 1 , JBP1, a newly characterized protein methyltransferase. |
| Score | Text |
|---|---|
| 0.9996 | In this report, ProteinHsl7p also is shown to be a methyltransferase. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9970 | Calf histones H2A and H4 and bovine myelin basic protein were methylated by ProteinHsl7p , whereas histones H1, H2B, and H3 and bovine cytochrome c were not. |
| 0.9893 | Calf histones H2A and ProteinH4 and bovine myelin basic protein were methylated by Hsl7p, whereas histones H1, H2B, and H3 and bovine cytochrome c were not. |
| 0.9845 | Calf histones H2A and H4 and bovine myelin basic protein were methylated by Hsl7p, whereas histones H1, ProteinH2B , and H3 and bovine cytochrome c were not. |
| 0.9780 | Calf histones H2A and H4 and bovine myelin basic protein were methylated by Hsl7p, whereas histones H1, H2B, and ProteinH3 and bovine cytochrome c were not. |
| 0.9716 | Calf histones H2A and H4 and bovine myelin basic protein were methylated by Hsl7p, whereas Proteinhistones H1 , H2B, and H3 and bovine cytochrome c were not. |
| 0.9619 | Calf Proteinhistones H2A and H4 and bovine myelin basic protein were methylated by Hsl7p, whereas histones H1, H2B, and H3 and bovine cytochrome c were not. |
| 0.9281 | Calf histones H2A and H4 and bovine myelin basic protein were methylated by Hsl7p, whereas histones H1, H2B, and H3 and bovine Proteincytochrome c were not. |
| 0.9184 | Calf histones H2A and H4 and bovine Proteinmyelin basic protein were methylated by Hsl7p, whereas histones H1, H2B, and H3 and bovine cytochrome c were not. |
| 0.6789 | Calf histones H2A and H4 and bovine myelin basic protein were Catalysismethylated by Hsl7p, whereas histones H1, H2B, and H3 and bovine cytochrome c were not. |
| Calf histones H2A and H4 and bovine myelin basic protein were Methylationmethylated by Hsl7p, whereas histones H1, H2B, and H3 and bovine cytochrome c were not. | |
| Score | Text |
|---|---|
| 0.9999 | We demonstrated that JBP1 can complement Saccharomyces cerevisiae with a disrupted HSL7 gene as judged by a reduction of the elongated bud phenotype, and a point mutation in the JBP1 S - adenosylmethionine consensus binding sequence eliminated all complementation by ProteinJBP1 . |
| 0.9999 | We demonstrated that ProteinJBP1 can complement Saccharomyces cerevisiae with a disrupted HSL7 gene as judged by a reduction of the elongated bud phenotype, and a point mutation in the JBP1 S - adenosylmethionine consensus binding sequence eliminated all complementation by JBP1. |
| 0.9997 | We demonstrated that JBP1 can complement Saccharomyces cerevisiae with a disrupted ProteinHSL7 gene as judged by a reduction of the elongated bud phenotype, and a point mutation in the JBP1 S - adenosylmethionine consensus binding sequence eliminated all complementation by JBP1. |
| 0.9994 | We demonstrated that JBP1 can complement Saccharomyces cerevisiae with a disrupted HSL7 gene as judged by a reduction of the elongated bud phenotype, and a point mutation in the ProteinJBP1 S - adenosylmethionine consensus binding sequence eliminated all complementation by JBP1. |
| Score | Text |
|---|---|
| 0.9998 | Therefore, we conclude the yeast protein Hsl7p is a sequence and functional homologue of ProteinJBP1 . |
| 0.9998 | Therefore, we conclude the yeast protein ProteinHsl7p is a sequence and functional homologue of JBP1. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9962 | Rapid induction of Proteinhistone hyperacetylation and cellular differentiation in human breast tumor cell lines following degradation of histone deacetylase - 1. |
| 0.9450 | Rapid induction of histone Acetylationhyperacetylation and cellular differentiation in human breast tumor cell lines following degradation of histone deacetylase - 1. |
| 0.6429 | Rapid induction of histone hyperacetylation and cellular differentiation in human breast tumor cell lines following degradation of Proteinhistone deacetylase - 1 . |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9385 | The cells accumulated lipid droplets, and the Proteincytokeratin 18 cytoskeleton was reorganized. |
| Score | Text |
|---|---|
| 0.9712 | AcetylationHyperacetylated histone H4 appeared within 2 h of the addition of quinidine to the medium, and levels were maximal by 24 h. |
| 0.9591 | Hyperacetylated Proteinhistone H4 appeared within 2 h of the addition of quinidine to the medium, and levels were maximal by 24 h. |
| Score | Text |
|---|---|
| 0.9877 | Quinidine - treated MCF - 7 cells showed elevated Proteinp21 ( WAF1 ) , hypophosphorylation and suppression of retinoblastoma protein, and down - regulation of cyclin D1, similar to the cell cycle response observed with cells induced to differentiate by histone deacetylase inhibitors, trichostatin A, and trapoxin. |
| 0.9867 | Quinidine - treated MCF - 7 cells showed elevated p21 ( WAF1 ), hypophosphorylation and suppression of retinoblastoma protein, and down - regulation of cyclin D1, similar to the cell cycle response observed with cells induced to differentiate by Proteinhistone deacetylase inhibitors, trichostatin A, and trapoxin. |
| 0.9713 | Quinidine - treated MCF - 7 cells showed elevated p21 ( WAF1 ), hypophosphorylation and suppression of Proteinretinoblastoma protein, and down - regulation of cyclin D1, similar to the cell cycle response observed with cells induced to differentiate by histone deacetylase inhibitors, trichostatin A, and trapoxin. |
| 0.9423 | Quinidine - treated MCF - 7 cells showed elevated p21 ( WAF1 ), hypophosphorylation and suppression of retinoblastoma protein, and down - regulation of Proteincyclin D1 , similar to the cell cycle response observed with cells induced to differentiate by histone deacetylase inhibitors, trichostatin A, and trapoxin. |
| 0.9187 | Quinidine - treated MCF - 7 cells showed elevated p21 ( WAF1 ), Phosphorylationhypophosphorylation and suppression of retinoblastoma protein, and down - regulation of cyclin D1, similar to the cell cycle response observed with cells induced to differentiate by histone deacetylase inhibitors, trichostatin A, and trapoxin. |
| Score | Text |
|---|---|
| 0.9988 | Quinidine did not show evidence for direct inhibition of Proteinhistone deacetylase enzymatic activity in vitro. |
| Score | Text |
|---|---|
| 0.9994 | ProteinHDAC1 was undetectable in MCF - 7 cells 30 min after addition of quinidine to the growth medium. |
| Score | Text |
|---|---|
| 0.9994 | The proteasome inhibitors MG - 132 and lactacystin completely protected ProteinHDAC1 from the action of quinidine. |
| Score | Text |
|---|---|
| 0.9998 | We conclude that quinidine is a breast tumor cell differentiating agent that causes the loss of ProteinHDAC1 via a proteasomal sensitive mechanism. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9996 | The ProteinKvLQT1 and minK subunits that coassemble to form I ( sK ) channels, contain potential N - glycosylation sites. |
| 0.9992 | The KvLQT1 and ProteinminK subunits that coassemble to form I ( sK ) channels, contain potential N - glycosylation sites. |
| Score | Text |
|---|---|
| 0.9930 | To examine the role of glycosylation in channel function, a Chinese hamster ovary cell line deficient in glycosylation ( Lec - 1 ) and its parental cell line ( Pro - 5 ) were transiently transfected with human KvLQT1 ( hKvLQT1 ) cDNA, alone and in combination with the rat Protein( rminK ) or human minK ( hminK ) cDNA. |
| 0.9878 | To examine the role of glycosylation in channel function, a Chinese hamster ovary cell line deficient in glycosylation ( Lec - 1 ) and its parental cell line ( Pro - 5 ) were transiently transfected with human ProteinKvLQT1 ( hKvLQT1 ) cDNA, alone and in combination with the rat ( rminK ) or human minK ( hminK ) cDNA. |
| 0.9802 | To examine the role of glycosylation in channel function, a Chinese hamster ovary cell line deficient in glycosylation ( Lec - 1 ) and its parental cell line ( Pro - 5 ) were transiently transfected with human KvLQT1 ( hKvLQT1 ) cDNA, alone and in combination with the rat ( rminK ) or human ProteinminK ( hminK ) cDNA. |
| 0.9755 | To examine the role of glycosylation in channel function, a Chinese hamster ovary cell line deficient in glycosylation ( Lec - 1 ) and its parental cell line ( Pro - 5 ) were transiently transfected with human KvLQT1 ( hKvLQT1 ) cDNA, alone and in combination with the rat ( rminK ) or human minK Protein( hminK ) cDNA. |
| 0.9669 | To examine the role of glycosylation in channel function, a Chinese hamster ovary cell line deficient in glycosylation ( Lec - 1 ) and its parental cell line ( Pro - 5 ) were transiently transfected with human KvLQT1 Protein( hKvLQT1 ) cDNA, alone and in combination with the rat ( rminK ) or human minK ( hminK ) cDNA. |
| 0.9427 | To examine the role of glycosylation in channel function, a Chinese hamster ovary cell line deficient in glycosylation ( Lec - 1 ) and its parental cell line ( Pro - 5 ) were transiently transfected with human KvLQT1 ( hKvLQT1 ) cDNA, alone and in combination with the rat ( rminK ) or human ProteinminK ( hminK ) cDNA. |
| 0.9248 | To examine the role of glycosylation in channel function, a Chinese hamster ovary cell line deficient in glycosylation ( Lec - 1 ) and its parental cell line ( Pro - 5 ) were transiently transfected with human ProteinKvLQT1 ( hKvLQT1 ) cDNA, alone and in combination with the rat ( rminK ) or human minK ( hminK ) cDNA. |
| 0.6275 | To examine the role of glycosylation in channel function, a Chinese hamster ovary cell line deficient in Glycosylationglycosylation ( Lec - 1 ) and its parental cell line ( Pro - 5 ) were transiently transfected with human KvLQT1 ( hKvLQT1 ) cDNA, alone and in combination with the rat ( rminK ) or human minK ( hminK ) cDNA. |
| Score | Text |
|---|---|
| 0.9996 | Functional KvLQT1 and I ( sK ) currents were expressed in both cell lines, although amplitudes were larger in Pro - 5 than Lec - 1 cells transfected with ProteinhKvLQT1 and hKvLQT1 / hminK. |
| 0.9995 | Functional KvLQT1 and I ( sK ) currents were expressed in both cell lines, although amplitudes were larger in Pro - 5 than Lec - 1 cells transfected with hKvLQT1 and ProteinhKvLQT1 / hminK . |
| 0.9994 | Functional ProteinKvLQT1 and I ( sK ) currents were expressed in both cell lines, although amplitudes were larger in Pro - 5 than Lec - 1 cells transfected with hKvLQT1 and hKvLQT1 / hminK. |
| Score | Text |
|---|---|
| 0.9997 | For I ( sK ), but not ProteinKvLQT1 , the voltage - dependence of activation was shifted to more positive voltages and the activation kinetics were slower in the Lec - 1 compared to the Pro - 5 cells. |
| Score | Text |
|---|---|
| 0.9997 | The effect of extracellular acidification on recombinant ProteinKvLQT1 and I ( sK ) currents was investigated in Pro - 5 and Lec - 1 cells. |
| Score | Text |
|---|---|
| 0.9998 | Changing external pH ( pH ( o ) ) from 7. 4 to 6. 0 significantly decreased the amplitude and increased the half - activation voltage ( V ( 1 / 2 ) ) of ProteinKvLQT1 currents in Pro - 5 and Lec - 1 cells. |
| Score | Text |
|---|---|
| 0.9998 | In Pro - 5 cells, decreasing pH ( o ) reduced I ( sK ) amplitude without increasing V ( 1 / 2 ), whether rminK or ProteinhminK was coexpressed with hKvLQT. |
| 0.9997 | In Pro - 5 cells, decreasing pH ( o ) reduced I ( sK ) amplitude without increasing V ( 1 / 2 ), whether ProteinrminK or hminK was coexpressed with hKvLQT. |
| 0.9997 | In Pro - 5 cells, decreasing pH ( o ) reduced I ( sK ) amplitude without increasing V ( 1 / 2 ), whether rminK or hminK was coexpressed with ProteinhKvLQT . |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9940 | Thus, oligosaccharides attached to the ProteinminK subunit affect not only the gating properties, but also the pH sensitivity of I ( sK ). |
| 0.9781 | Thus, Entityoligosaccharides attached to the minK subunit affect not only the gating properties, but also the pH sensitivity of I ( sK ). |
| 0.8683 | Thus, oligosaccharides Glycosylationattached to the minK subunit affect not only the gating properties, but also the pH sensitivity of I ( sK ). |
| Score | Text |
|---|---|
| 0.9461 | A novel post - translational modification of yeast Proteinelongation factor 1A . Methylesterification at the C terminus. |
| 0.6711 | A novel post - translational modification of yeast elongation factor 1A. Methylesterification at the C Entityterminus. |
| 0.7514 | A novel post - translational modification of yeast elongation factor 1A. Methylesterification at the C Entityterminus . |
| 0.6105 | A novel post - translational modification of yeast elongation factor 1A. Methylesterification at the C terminus Entity. |
| 0.5136 | A novel post - translational modification of yeast elongation factor 1A. MethylationMethylesterification at the C terminus. |
| A novel post - translational modification of yeast elongation factor 1A. Methylesterification Methylationat the C terminus. | |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9972 | Peptide sequence analysis of the purified methylated protein revealed that it is eukaryotic elongation factor 1A ( eEF1A, formerly ProteinEF - 1alpha ) , the protein that forms a complex with GTP and aminoacyl - tRNAs for binding to the ribosomal A site during protein translation. |
| 0.9606 | Peptide sequence analysis of the purified methylated protein revealed that it is eukaryotic elongation factor 1A Protein( eEF1A , formerly EF - 1alpha ), the protein that forms a complex with GTP and aminoacyl - tRNAs for binding to the ribosomal A site during protein translation. |
| 0.8489 | Peptide sequence analysis of the purified methylated protein revealed that it is eukaryotic Proteinelongation factor 1A ( eEF1A, formerly EF - 1alpha ), the protein that forms a complex with GTP and aminoacyl - tRNAs for binding to the ribosomal A site during protein translation. |
| Score | Text |
|---|---|
| 0.9971 | Previous studies have shown that ProteineEF1A is methylated on several internal lysine residues to give mono -, di -, and tri - N - epsilon - methyl - lysine derivatives. |
| 0.9474 | Previous studies have shown that eEF1A is Methylationmethylated on several internal lysine residues to give mono -, di -, and tri - N - epsilon - methyl - lysine derivatives. |
| 0.9245 | Previous studies have shown that eEF1A is methylated on several internal Entitylysine residues to give mono -, di -, and tri - N - epsilon - methyl - lysine derivatives. |
| 0.6905 | Previous studies have shown that eEF1A is methylated on several internal Entitylysine residues to give mono -, di -, and tri - N - epsilon - methyl - lysine derivatives. |
| Score | Text |
|---|---|
| 0.5146 | We confirm this finding but also detect Methylationmethylation that is released as volatile methyl groups after base hydrolysis, characteristic of ester linkages. |
| Score | Text |
|---|---|
| 0.9973 | In cycloheximide - treated cells, methyl esterified ProteineEF1A was detected largely in the ribosome and polysome fractions ; little or no methylated protein was found in the soluble fraction. |
| 0.9578 | In cycloheximide - treated cells, methyl esterified eEF1A was detected largely in the ribosome and polysome fractions ; little or no Methylationmethylated protein was found in the soluble fraction. |
| 0.8917 | In cycloheximide - treated cells, Methylationmethyl esterified eEF1A was detected largely in the ribosome and polysome fractions ; little or no methylated protein was found in the soluble fraction. |
| 0.9208 | In cycloheximide - treated cells, Methylationmethyl esterified eEF1A was detected largely in the ribosome and polysome fractions ; little or no methylated protein was found in the soluble fraction. |
| 0.9066 | In cycloheximide - treated cells, methyl Methylationesterified eEF1A was detected largely in the ribosome and polysome fractions ; little or no methylated protein was found in the soluble fraction. |
| Score | Text |
|---|---|
| 0.9985 | Because the base - labile, volatile [ methyl - ( 3 ) H ] radioactivity of ProteineEF1A could be released by trypsin treatment but not by carboxypeptidase Y or chymotrypsin treatment, we suggest that the methyl ester is present on the alpha - carboxyl group of its C - terminal lysine residue. |
| 0.9895 | Because the base - labile, volatile [ methyl - ( 3 ) H ] radioactivity of eEF1A could be released by trypsin treatment but not by carboxypeptidase Y or Proteinchymotrypsin treatment, we suggest that the methyl ester is present on the alpha - carboxyl group of its C - terminal lysine residue. |
| 0.9726 | Because the base - labile, volatile [ methyl - ( 3 ) H ] radioactivity of eEF1A could be released by trypsin treatment but not by Proteincarboxypeptidase Y or chymotrypsin treatment, we suggest that the methyl ester is present on the alpha - carboxyl group of its C - terminal lysine residue. |
| Score | Text |
|---|---|
| 0.9822 | From the results of pulse - chase experiments using radiolabeled intact yeast cells, we find that the N - methylated lysine residues of ProteineEF1A are stable over 4 h, whereas the eEF1A carboxyl methyl ester has a half - life of less than 10 min. |
| 0.9752 | From the results of pulse - chase experiments using radiolabeled intact yeast cells, we find that the N - methylated lysine residues of eEF1A are stable over 4 h, whereas the ProteineEF1A carboxyl methyl ester has a half - life of less than 10 min. |
| 0.9606 | From the results of pulse - chase experiments using radiolabeled intact yeast cells, we find that the N - methylated Entitylysine residues of eEF1A are stable over 4 h, whereas the eEF1A carboxyl methyl ester has a half - life of less than 10 min. |
| 0.9305 | From the results of pulse - chase experiments using radiolabeled intact yeast cells, we find that the MethylationN - methylated lysine residues of eEF1A are stable over 4 h, whereas the eEF1A carboxyl methyl ester has a half - life of less than 10 min. |
| 0.9633 | From the results of pulse - chase experiments using radiolabeled intact yeast cells, we find that the N - methylated Entitylysine residues of eEF1A are stable over 4 h, whereas the eEF1A carboxyl methyl ester has a half - life of less than 10 min. |
| Score | Text |
|---|---|
| 0.9869 | The rapid turnover of the methyl ester suggests that the methylation / demethylation of ProteineEF1A at the C - terminal carboxyl group may represent a novel mode of regulation of the activity of this protein in yeast. |
| 0.8168 | The rapid turnover of the methyl ester suggests that the methylation / demethylation of eEF1A at the EntityC - terminal carboxyl group may represent a novel mode of regulation of the activity of this protein in yeast. |
| 0.6890 | The rapid turnover of the methyl ester suggests that the Methylationmethylation / demethylation of eEF1A at the C - terminal carboxyl group may represent a novel mode of regulation of the activity of this protein in yeast. |
| 0.6115 | The rapid turnover of the methyl ester suggests that the methylation / demethylation of eEF1A at the EntityC - terminal carboxyl group may represent a novel mode of regulation of the activity of this protein in yeast. |
| 0.5162 | The rapid turnover of the methyl ester suggests that the methylation / demethylation of eEF1A at the EntityC - terminal carboxyl group may represent a novel mode of regulation of the activity of this protein in yeast. |
| The rapid turnover of the methyl ester suggests that the Demethylationmethylation / demethylation of eEF1A at the C - terminal carboxyl group may represent a novel mode of regulation of the activity of this protein in yeast. | |
| Score | Text |
|---|---|
| 0.9997 | Decreased UDP - GlcNAc levels abrogate proliferation control in ProteinEMeg32 - deficient cells. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9974 | We have recently identified the murine glucosamine - 6 - phosphate ( GlcN6P ) acetyltransferase, ProteinEMeg32 , as a developmentally regulated enzyme on the route to UDP - N : - acetylglucosamine ( UDP - GlcNAc ). |
| We have recently identified the murine Proteinglucosamine - 6 - phosphate ( GlcN6P ) acetyltransferase , EMeg32, as a developmentally regulated enzyme on the route to UDP - N : - acetylglucosamine ( UDP - GlcNAc ). | |
| Score | Text |
|---|---|
| 0.9995 | Here we describe embryos and cells that have the ProteinEMeg32 gene inactivated by homologous recombination. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9943 | In vitro differentiated ProteinEMeg32 ( - / - ) ES cells show reduced proliferation. |
| Score | Text |
|---|---|
| 0.9998 | Mouse embryonic fibroblasts ( MEFs ) deficient for EMeg32 exhibit defects in proliferation and adhesiveness, which could be complemented by stable re - expression of ProteinEMeg32 or by nutritional restoration of intracellular UDP - GlcNAc levels. |
| 0.9997 | Mouse embryonic fibroblasts ( MEFs ) deficient for ProteinEMeg32 exhibit defects in proliferation and adhesiveness, which could be complemented by stable re - expression of EMeg32 or by nutritional restoration of intracellular UDP - GlcNAc levels. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9994 | Interestingly, growth - impaired EMeg32 ( - / - ) MEFs withstand a number of apoptotic stimuli and express activated ProteinPKB / AKT . |
| 0.9876 | Interestingly, growth - impaired ProteinEMeg32 ( - / - ) MEFs withstand a number of apoptotic stimuli and express activated PKB / AKT. |
| Score | Text |
|---|---|
| 0.9572 | Thus, ProteinEMeg32 - dependent UDP - GlcNAc levels influence cell cycle progression and susceptibility to apoptotic stimuli. |
| Score | Text |
|---|---|
| 0.9851 | Post - translational hydroxylation at the EntityN - terminus of the prion protein reveals presence of PPII structure in vivo. |
| 0.9833 | Post - translational Hydroxylationhydroxylation at the N - terminus of the prion protein reveals presence of PPII structure in vivo. |
| 0.8842 | Post - translational hydroxylation at the N - terminus of the Proteinprion protein reveals presence of PPII structure in vivo. |
| 0.5360 | Post - translational hydroxylation at the N - terminus of the Proteinprion protein reveals presence of PPII structure in vivo. |
| Score | Text |
|---|---|
| 0.9991 | The transmissible spongiform encephalopathies are characterized by conversion of a host protein, ProteinPrP ( C ) ( cellular prion protein ), to a protease - resistant isoform, PrP ( Sc ) ( prion protein scrapie isoform ). |
| 0.9858 | The transmissible spongiform encephalopathies are characterized by conversion of a host protein, PrP ( C ) ( cellular prion protein ), to a protease - resistant isoform, ProteinPrP ( Sc ) ( prion protein scrapie isoform ). |
| 0.9844 | The transmissible spongiform encephalopathies are characterized by conversion of a host protein, PrP ( C ) ( cellular Proteinprion protein ) , to a protease - resistant isoform, PrP ( Sc ) ( prion protein scrapie isoform ). |
| 0.8187 | The transmissible spongiform encephalopathies are characterized by conversion of a host protein, PrP ( C ) ( cellular prion protein ), to a protease - resistant isoform, ProteinPrP ( Sc ) ( prion protein scrapie isoform ). |
| The transmissible spongiform encephalopathies are characterized by conversion of a host protein, PrP ( C ) ( cellular prion protein ), to a protease - resistant isoform, PrP ( Sc ) Protein( prion protein scrapie isoform ). | |
| Score | Text |
|---|---|
| 0.9991 | The importance of the highly flexible, N - terminal region of ProteinPrP has recently become more widely appreciated, particularly the biological activities associated with its metal ion - binding domain and its potential to form a poly ( L - proline ) II ( PPII ) helix. |
| Score | Text |
|---|---|
| 0.9977 | Circular dichroism spectroscopy of an N - terminal peptide, ProteinPrP ( 37 - 53 ) , showed that the PPII helix is formed in aqueous buffer ; as it also contains an Xaa - Pro - Gly consensus sequence, it may act as a substrate for the collagen - modifying enzyme prolyl 4 - hydroxylase. |
| Score | Text |
|---|---|
| 0.9999 | Direct evidence for this modification was obtained by mass spectrometry and Edman sequencing in recombinant mouse ProteinPrP secreted from stably transfected Chinese hamster ovary cells. |
| Score | Text |
|---|---|
| 0.9822 | Almost complete conversion of proline to 4 - hydroxyproline occurs specifically at residue Pro44 of this murine protein ; the same hydroxylated residue was detected, at lower levels, in ProteinPrP ( Sc ) from the brains of scrapie - infected mice. |
| 0.9815 | Almost complete conversion of proline to 4 - hydroxyproline occurs specifically at residue Pro44 of this murine protein ; the same Hydroxylationhydroxylated residue was detected, at lower levels, in PrP ( Sc ) from the brains of scrapie - infected mice. |
| 0.9782 | Almost complete conversion of proline to 4 - hydroxyproline occurs specifically at residue EntityPro44 of this murine protein ; the same hydroxylated residue was detected, at lower levels, in PrP ( Sc ) from the brains of scrapie - infected mice. |
| 0.8374 | Almost complete Hydroxylationconversion of proline to 4 - hydroxyproline occurs specifically at residue Pro44 of this murine protein ; the same hydroxylated residue was detected, at lower levels, in PrP ( Sc ) from the brains of scrapie - infected mice. |
| Score | Text |
|---|---|
| 0.9961 | Cation binding and / or post - translational hydroxylation of this region of ProteinPrP may regulate its role in the physiology and pathobiology of the cell. |
| 0.9453 | Cation binding and / or post - translational Hydroxylationhydroxylation of this region of PrP may regulate its role in the physiology and pathobiology of the cell. |
| Score | Text |
|---|---|
| 0.9998 | Carboxymethylation of the PP2A catalytic subunit in Saccharomyces cerevisiae is required for efficient interaction with the B - type subunits Cdc55p and ProteinRts1p . |
| 0.9998 | Carboxymethylation of the PP2A catalytic subunit in Saccharomyces cerevisiae is required for efficient interaction with the B - type subunits ProteinCdc55p and Rts1p. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9987 | We have used the budding yeast Saccharomyces cerevisiae as a model system to investigate the hypothesis that covalent modification of the C subunit Protein( Pph21p / Pph22p ) carboxyl terminus modulates PP2A complex formation. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9999 | First, S. cerevisiae cells were generated whose survival depended on the expression of different carboxyl - terminal ProteinPph21p mutants. |
| Score | Text |
|---|---|
| 0.9643 | Second, the major S. cerevisiae methyltransferase Protein( Ppm1p ) that catalyzes the methylation of the PP2A C subunit carboxyl - terminal leucine was identified, and cells deleted for this methyltransferase were utilized for our studies. |
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| 0.9997 | Our results demonstrate that binding of the yeast B subunit, Cdc55p, to Pph21p was disrupted by either acidic substitution of potential carboxyl - terminal phosphorylation sites on ProteinPph21p or by deletion of the gene for Ppm1p. |
| 0.9996 | Our results demonstrate that binding of the yeast B subunit, Cdc55p, to Pph21p was disrupted by either acidic substitution of potential carboxyl - terminal phosphorylation sites on Pph21p or by deletion of the gene for ProteinPpm1p . |
| 0.9996 | Our results demonstrate that binding of the yeast B subunit, ProteinCdc55p , to Pph21p was disrupted by either acidic substitution of potential carboxyl - terminal phosphorylation sites on Pph21p or by deletion of the gene for Ppm1p. |
| 0.9996 | Our results demonstrate that binding of the yeast B subunit, Cdc55p, to ProteinPph21p was disrupted by either acidic substitution of potential carboxyl - terminal phosphorylation sites on Pph21p or by deletion of the gene for Ppm1p. |
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|---|---|
| 0.9998 | Loss of Cdc55p association was accompanied in each case by a large reduction in binding of the yeast A subunit, ProteinTpd3p , to Pph21p. |
| 0.9995 | Loss of ProteinCdc55p association was accompanied in each case by a large reduction in binding of the yeast A subunit, Tpd3p, to Pph21p. |
| 0.9995 | Loss of Cdc55p association was accompanied in each case by a large reduction in binding of the yeast A subunit, Tpd3p, to ProteinPph21p . |
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| 0.9998 | Moreover, decreased Cdc55p and Tpd3p binding invariably resulted in nocodazole sensitivity, a known phenotype of CDC55 or ProteinTPD3 deletion. |
| 0.9998 | Moreover, decreased ProteinCdc55p and Tpd3p binding invariably resulted in nocodazole sensitivity, a known phenotype of CDC55 or TPD3 deletion. |
| 0.9997 | Moreover, decreased Cdc55p and Tpd3p binding invariably resulted in nocodazole sensitivity, a known phenotype of ProteinCDC55 or TPD3 deletion. |
| 0.9997 | Moreover, decreased Cdc55p and ProteinTpd3p binding invariably resulted in nocodazole sensitivity, a known phenotype of CDC55 or TPD3 deletion. |
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| 0.9992 | Furthermore, loss of methylation also greatly reduced the association of another yeast B - type subunit, ProteinRts1p . |
| 0.4138 | Furthermore, loss of DNA_methylationmethylation also greatly reduced the association of another yeast B - type subunit, Rts1p. |
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| 0.9986 | Thus, methylation of ProteinPph21p is important for formation of PP2A trimeric and dimeric complexes, and consequently, for PP2A function. |
| 0.7999 | Thus, Methylationmethylation of Pph21p is important for formation of PP2A trimeric and dimeric complexes, and consequently, for PP2A function. |
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| 0.9982 | OUTCOME MEASURES : Safety parameters, evaluated at each dose level, included measurement of total testosterone, free testosterone, dihydrotestosterone, estradiol, cortisol, thyroxin and Proteininsulin levels. |
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| 0.9362 | ProteinAureusidin synthase : a polyphenol oxidase homolog responsible for flower coloration. |
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| 0.9690 | The enzyme Protein( aureusidin synthase ) is a 39 - kilodalton, copper - containing glycoprotein catalyzing the hydroxylation and / or oxidative cyclization of the precursor chalcones, 2 ', 4 ', 6 ', 4 - tetrahydroxychalcone and 2 ', 4 ', 6 ', 3, 4 - pentahydroxychalcone. |
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| 0.9674 | The complementary DNA encoding Proteinaureusidin synthase is expressed in the petals of aurone - containing varieties. |
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| 0.9838 | DNA sequence analysis revealed that Proteinaureusidin synthase belongs to the plant polyphenol oxidase family, providing an unequivocal example of the function of the polyphenol oxidase homolog in plants, i. e., flower coloration. |
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|---|---|
| 0.9934 | ProteinE - cadherin expression is silenced by 5'CpG island methylation in acute leukemia. |
| 0.9906 | E - cadherin expression is silenced by 5'CpG island DNA_methylationmethylation in acute leukemia. |
| 0.5636 | E - cadherin expression is silenced by Entity5'CpG island methylation in acute leukemia. |
| 0.5725 | E - cadherin expression is silenced by 5 ' EntityCpG island methylation in acute leukemia. |
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| 0.9964 | ProteinE - Cadherin is a transmembrane glycoprotein that mediates Ca2 + - dependent intercellular adhesion in normal epithelium. |
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| 0.9996 | In tumors of epithelial origin, ProteinE - cadherin expression frequently is reduced, an event that contributes to tumor invasion and metastasis. |
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| 0.9996 | The role of ProteinE - cadherin in hematopoietic tissues is less clear. |
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| 0.9996 | In normal bone marrow, ProteinE - cadherin is expressed on erythroid progenitors, CD34 + stem cells, and stromal cells, where it likely contributes to intercellular interactions during hematopoiesis. |
| 0.9993 | In normal bone marrow, E - cadherin is expressed on erythroid progenitors, ProteinCD34 + stem cells, and stromal cells, where it likely contributes to intercellular interactions during hematopoiesis. |
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|---|---|
| 0.9914 | In this study, we used a nested - PCR approach to examine the DNA_methylationmethylation status of the E - cadherin 5'CpG island in blood and bone marrow samples from normal donors and in bone marrow from patients with acute leukemia. |
| 0.9515 | In this study, we used a nested - PCR approach to examine the methylation status of the ProteinE - cadherin 5'CpG island in blood and bone marrow samples from normal donors and in bone marrow from patients with acute leukemia. |
| 0.7872 | In this study, we used a nested - PCR approach to examine the methylation status of the E - cadherin Entity5'CpG island in blood and bone marrow samples from normal donors and in bone marrow from patients with acute leukemia. |
| 0.8178 | In this study, we used a nested - PCR approach to examine the methylation status of the E - cadherin 5 ' EntityCpG island in blood and bone marrow samples from normal donors and in bone marrow from patients with acute leukemia. |
| 0.7121 | In this study, we used a nested - PCR approach to examine the methylation status of the E - cadherin 5 ' EntityCpG island in blood and bone marrow samples from normal donors and in bone marrow from patients with acute leukemia. |
| 0.5629 | In this study, we used a nested - PCR approach to examine the methylation status of the E - cadherin Entity5'CpG island in blood and bone marrow samples from normal donors and in bone marrow from patients with acute leukemia. |
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|---|---|
| 0.9986 | In normal peripheral blood mononuclear cells and bone marrow, ProteinE - cadherin was completely unmethylated. |
| 0.9065 | In normal peripheral blood mononuclear cells and bone marrow, E - cadherin was completely DNA_methylationunmethylated . |
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| 0.9995 | Immunoblotting confirmed ProteinE - cadherin protein expression in two lymphoblastoid cell lines derived from normal donors. |
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| 0.9978 | In contrast, ProteinE - cadherin was aberrantly methylated in 4 of 4 ( 100 % ) leukemia cell lines, 14 of 44 ( 32 % ) acute myelogenous leukemias, and 18 of 33 ( 53 % ) acute lymphoblastic leukemias. |
| 0.9778 | In contrast, E - cadherin was aberrantly DNA_methylationmethylated in 4 of 4 ( 100 % ) leukemia cell lines, 14 of 44 ( 32 % ) acute myelogenous leukemias, and 18 of 33 ( 53 % ) acute lymphoblastic leukemias. |
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| 0.9793 | Genomic bisulfite sequencing of primary leukemias confirmed dense DNA_methylationmethylation across the CpG island. |
| 0.7436 | Genomic bisulfite sequencing of primary leukemias confirmed dense methylation across the EntityCpG island . |
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|---|---|
| 0.9986 | Methylation was associated with loss of ProteinE - cadherin RNA and protein in leukemia cell lines and primary leukemias. |
| 0.9860 | DNA_methylationMethylation was associated with loss of E - cadherin RNA and protein in leukemia cell lines and primary leukemias. |
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| 0.9989 | Following treatment with 5 - aza - 2'- deoxycytidine, a methylated leukemia cell line expressed both ProteinE - cadherin transcript and protein. |
| 0.9633 | Following treatment with 5 - aza - 2'- deoxycytidine, a DNA_methylationmethylated leukemia cell line expressed both E - cadherin transcript and protein. |
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| 0.9992 | Our results show that methylation of ProteinE - cadherin occurs commonly in acute leukemia and suggests a hypothesis for E - cadherin down - regulation in leukemogenesis. |
| 0.9991 | Our results show that methylation of E - cadherin occurs commonly in acute leukemia and suggests a hypothesis for ProteinE - cadherin down - regulation in leukemogenesis. |
| 0.9513 | Our results show that DNA_methylationmethylation of E - cadherin occurs commonly in acute leukemia and suggests a hypothesis for E - cadherin down - regulation in leukemogenesis. |
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| 0.9882 | Hypoglycosylated forms of Proteinalpha1 - antitrypsin have been detected by Western blot in serum from CDG Ia patients. |
| 0.7849 | GlycosylationHypoglycosylated forms of alpha1 - antitrypsin have been detected by Western blot in serum from CDG Ia patients. |
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| 0.9891 | In contrast we were not able to detect hypoglycosylation in Proteinalpha1 - antitrypsin synthesized by fibroblasts, keratinocytes, enterocytes, and leukocytes. |
| 0.8951 | In contrast we were not able to detect Glycosylationhypoglycosylation in alpha1 - antitrypsin synthesized by fibroblasts, keratinocytes, enterocytes, and leukocytes. |
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| 0.9983 | Similarly no hypoglycosylation was detectable in a membrane - associated N - linked glycoprotein, the facilitative glucose transporter ProteinGLUT - 1 and also in serum immunoglobulin G isolated from sera of CDG Ia patients. |
| 0.8071 | Similarly no Glycosylationhypoglycosylation was detectable in a membrane - associated N - linked glycoprotein, the facilitative glucose transporter GLUT - 1 and also in serum immunoglobulin G isolated from sera of CDG Ia patients. |
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| 0.9993 | Molecular cloning and characterization of ProteinCHM1L , a novel membrane molecule similar to chondromodulin - I. |
| 0.9965 | Molecular cloning and characterization of CHM1L, a novel membrane molecule similar to Proteinchondromodulin - I . |
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|---|---|
| 0.9790 | Chondromodulin - I Protein( ChM - I ) is a cartilage - specific glycoprotein that stimulates the growth of chondrocytes and inhibits the tube formation of endothelial cells. |
| 0.9666 | ProteinChondromodulin - I ( ChM - I ) is a cartilage - specific glycoprotein that stimulates the growth of chondrocytes and inhibits the tube formation of endothelial cells. |
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| 0.9996 | In the present study, we identified a novel ChM - I like molecule, designated ProteinChM1L . |
| 0.9846 | In the present study, we identified a novel ProteinChM - I like molecule, designated ChM1L. |
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| 0.9999 | Cloning of full length cDNAs of human, mouse, and rat ProteinChM1L revealed that ChM1L encodes 317 amino acids novel type II transmembrane protein. |
| 0.9998 | Cloning of full length cDNAs of human, mouse, and rat ChM1L revealed that ProteinChM1L encodes 317 amino acids novel type II transmembrane protein. |
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| 0.9980 | ProteinChM1L protein was expressed on the cell surface as N - glycosylated and non - N - glycosylated protein with molecular mass of 45 and 40 kDa, respectively. |
| 0.9895 | ChM1L protein was expressed on the cell surface as GlycosylationN - glycosylated and non - N - glycosylated protein with molecular mass of 45 and 40 kDa, respectively. |
| 0.9871 | ChM1L protein was expressed on the cell surface as N - glycosylated and Glycosylationnon - N - glycosylated protein with molecular mass of 45 and 40 kDa, respectively. |
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| 0.9993 | In adult mouse tissues, ProteinChM1L mRNA was highly expressed in eye, skeletal muscle, and whole rib. |
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| 0.9988 | The temporal pattern of ProteinChM1L mRNA was examined using whole embryo at day 10 to 19 of gestation. |
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| 0.9990 | After day 11, ProteinChM1L mRNA was detected and its level was progressively elevated in association with development of mouse embryo. |
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| 0.9998 | These data suggest that ChM1L is a novel membrane molecule which is similar to ProteinChM - I that plays a regulatory role in eye, skeletal muscle, and development of embryo. |
| 0.9992 | These data suggest that ProteinChM1L is a novel membrane molecule which is similar to ChM - I that plays a regulatory role in eye, skeletal muscle, and development of embryo. |
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| 0.9886 | A chimeric CS - hemoagglutinin 1 ( HA1 ), obtained by adding the nine amino acid viral epitope Proteinhemoagglutinin to the carboxy terminal of CS and shown to be correctly segregated to skeletal muscle jSR [ A. |
| 0.9843 | A chimeric CS - hemoagglutinin 1 Protein( HA1 ) , obtained by adding the nine amino acid viral epitope hemoagglutinin to the carboxy terminal of CS and shown to be correctly segregated to skeletal muscle jSR [ A. |
| 0.9049 | A chimeric ProteinCS - hemoagglutinin 1 ( HA1 ), obtained by adding the nine amino acid viral epitope hemoagglutinin to the carboxy terminal of CS and shown to be correctly segregated to skeletal muscle jSR [ A. |
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| 0.9976 | To test this hypothesis, ProteinCS - HA1DeltaGly , a mutant in which the unique N - glycosylation site Asn316 was changed to Ile, was engineered by site - directed mutagenesis. |
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| 0.9989 | The expression and intracellular localization of ProteinCS - HA1DeltaGly was studied by double - labeling epifluorescence by means of antibodies against either CS, HA1, or the ryanodine receptor calcium release channel. |
| 0.9979 | The expression and intracellular localization of CS - HA1DeltaGly was studied by double - labeling epifluorescence by means of antibodies against either CS, ProteinHA1 , or the ryanodine receptor calcium release channel. |
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|---|---|
| 0.9981 | ProteinCS - HA1DeltaGly was expressed and retained to ER and ER / sarcoplasmic reticulum of HeLa cells and myotubes, respectively, and expressed, sorted, and correctly segregated to jSR of regenerating soleus muscle fibers. |
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| 0.8673 | Targeting of HIF - alpha to the Proteinvon Hippel - Lindau ubiquitylation complex by O2 - regulated prolyl hydroxylation. |
| 0.6717 | Targeting of HIF - alpha to the von ProteinHippel - Lindau ubiquitylation complex by O2 - regulated prolyl hydroxylation. |
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| 0.9720 | In oxygenated and iron replete cells, HIF - alpha subunits are rapidly destroyed by a mechanism that involves ubiquitylation by the von Hippel - Lindau tumor suppressor Protein( pVHL ) E3 ligase complex. |
| 0.9280 | In oxygenated and iron replete cells, HIF - alpha subunits are rapidly destroyed by a mechanism that involves ubiquitylation by the Proteinvon Hippel - Lindau tumor suppressor ( pVHL ) E3 ligase complex. |
| 0.8724 | In oxygenated and iron replete cells, HIF - alpha subunits are rapidly destroyed by a mechanism that involves ubiquitylation by the von ProteinHippel - Lindau tumor suppressor ( pVHL ) E3 ligase complex. |
| 0.8001 | In oxygenated and iron replete cells, HIF - alpha subunits are rapidly destroyed by a mechanism that involves Ubiquitinationubiquitylation by the von Hippel - Lindau tumor suppressor ( pVHL ) E3 ligase complex. |
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|---|---|
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| 0.9977 | Here we show that the interaction between human ProteinpVHL and a specific domain of the HIF - 1alpha subunit is regulated through hydroxylation of a proline residue ( HIF - 1alpha P564 ) by an enzyme we have termed HIF - alpha prolyl - hydroxylase ( HIF - PH ). |
| 0.9930 | Here we show that the interaction between human pVHL and a specific domain of the ProteinHIF - 1alpha subunit is regulated through hydroxylation of a proline residue ( HIF - 1alpha P564 ) by an enzyme we have termed HIF - alpha prolyl - hydroxylase ( HIF - PH ). |
| 0.9523 | Here we show that the interaction between human pVHL and a specific domain of the HIF - 1alpha subunit is regulated through hydroxylation of a proline residue Protein( HIF - 1alpha P564 ) by an enzyme we have termed HIF - alpha prolyl - hydroxylase ( HIF - PH ). |
| 0.9316 | Here we show that the interaction between human pVHL and a specific domain of the HIF - 1alpha subunit is regulated through hydroxylation of a proline residue ( HIF - 1alpha EntityP564 ) by an enzyme we have termed HIF - alpha prolyl - hydroxylase ( HIF - PH ). |
| 0.9171 | Here we show that the interaction between human pVHL and a specific domain of the HIF - 1alpha subunit is regulated through Hydroxylationhydroxylation of a proline residue ( HIF - 1alpha P564 ) by an enzyme we have termed HIF - alpha prolyl - hydroxylase ( HIF - PH ). |
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| 0.9980 | HIFalpha targeted for ProteinVHL - mediated destruction by proline hydroxylation : implications for O2 sensing. |
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| 0.9888 | In the presence of oxygen, HIF is targeted for destruction by an E3 Proteinubiquitin ligase containing the von Hippel - Lindau tumor suppressor protein ( pVHL ). |
| 0.9856 | In the presence of oxygen, HIF is targeted for destruction by an E3 ubiquitin ligase containing the von Hippel - Lindau tumor suppressor protein Protein( pVHL ) . |
| 0.8214 | In the presence of oxygen, HIF is targeted for destruction by an E3 ubiquitin ligase containing the Proteinvon Hippel - Lindau tumor suppressor protein ( pVHL ). |
| 0.6451 | In the presence of oxygen, HIF is targeted for destruction by an E3 ubiquitin ligase containing the von ProteinHippel - Lindau tumor suppressor protein ( pVHL ). |
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|---|---|
| 0.9990 | We found that human ProteinpVHL binds to a short HIF - derived peptide when a conserved proline residue at the core of this peptide is hydroxylated. |
| 0.7480 | We found that human pVHL binds to a short HIF - derived peptide when a conserved proline residue at the core of this peptide is Hydroxylationhydroxylated . |
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| 0.9946 | We analyzed 100 sporadic and 3 hereditary pancreatic ductal adenocarcinomas for MSI, and high - frequency MSI ( MSI - H ) and low - frequency MSI ( MSI - L ) tumors were further analyzed for frameshift mutations of possible target genes and for Entitypromoter methylation and mutation of DNA MMR genes, including hMLH1, hMSH2, hMSH3, and hMSH6 genes. |
| 0.9939 | We analyzed 100 sporadic and 3 hereditary pancreatic ductal adenocarcinomas for MSI, and high - frequency MSI ( MSI - H ) and low - frequency MSI ( MSI - L ) tumors were further analyzed for frameshift mutations of possible target genes and for promoter methylation and mutation of DNA MMR genes, including hMLH1, ProteinhMSH2 , hMSH3, and hMSH6 genes. |
| 0.9931 | We analyzed 100 sporadic and 3 hereditary pancreatic ductal adenocarcinomas for MSI, and high - frequency MSI ( MSI - H ) and low - frequency MSI ( MSI - L ) tumors were further analyzed for frameshift mutations of possible target genes and for promoter methylation and mutation of DNA MMR genes, including ProteinhMLH1 , hMSH2, hMSH3, and hMSH6 genes. |
| 0.9926 | We analyzed 100 sporadic and 3 hereditary pancreatic ductal adenocarcinomas for MSI, and high - frequency MSI ( MSI - H ) and low - frequency MSI ( MSI - L ) tumors were further analyzed for frameshift mutations of possible target genes and for promoter methylation and mutation of DNA MMR genes, including hMLH1, hMSH2, ProteinhMSH3 , and hMSH6 genes. |
| 0.9919 | We analyzed 100 sporadic and 3 hereditary pancreatic ductal adenocarcinomas for MSI, and high - frequency MSI ( MSI - H ) and low - frequency MSI ( MSI - L ) tumors were further analyzed for frameshift mutations of possible target genes and for promoter methylation and mutation of DNA MMR genes, including hMLH1, hMSH2, hMSH3, and ProteinhMSH6 genes. |
| 0.9902 | We analyzed 100 sporadic and 3 hereditary pancreatic ductal adenocarcinomas for MSI, and high - frequency MSI ( MSI - H ) and low - frequency MSI ( MSI - L ) tumors were further analyzed for frameshift mutations of possible target genes and for promoter DNA_methylationmethylation and mutation of DNA MMR genes, including hMLH1, hMSH2, hMSH3, and hMSH6 genes. |
| 0.6006 | We analyzed 100 sporadic and 3 hereditary pancreatic ductal adenocarcinomas for MSI, and high - frequency MSI ( MSI - H ) and low - frequency MSI ( MSI - L ) tumors were further analyzed for frameshift mutations of possible target genes and for DNA_methylationpromoter methylation and mutation of DNA MMR genes, including hMLH1, hMSH2, hMSH3, and hMSH6 genes. |
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| 0.9996 | MSI - H tumors were significantly associated with poor differentiation and the presence of wild - type K - RAS and Proteinp53 genes. |
| 0.9989 | MSI - H tumors were significantly associated with poor differentiation and the presence of wild - type ProteinK - RAS and p53 genes. |
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|---|---|
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| 0.9990 | Frameshift mutations of hMSH3, ProteinhMLH3 , BRCA - 2, TGF - beta type II receptor, and BAX genes were detected in MSI - H tumors. |
| 0.9989 | Frameshift mutations of hMSH3, hMLH3, BRCA - 2, TGF - beta type II receptor, and ProteinBAX genes were detected in MSI - H tumors. |
| 0.9988 | Frameshift mutations of ProteinhMSH3 , hMLH3, BRCA - 2, TGF - beta type II receptor, and BAX genes were detected in MSI - H tumors. |
| 0.9721 | Frameshift mutations of hMSH3, hMLH3, ProteinBRCA - 2 , TGF - beta type II receptor, and BAX genes were detected in MSI - H tumors. |
| 0.8722 | Frameshift mutations of hMSH3, hMLH3, BRCA - 2, ProteinTGF - beta type II receptor , and BAX genes were detected in MSI - H tumors. |
| 0.7320 | Frameshift mutations of hMSH3, hMLH3, BRCA - 2, TGF - beta Proteintype II receptor , and BAX genes were detected in MSI - H tumors. |
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|---|---|
| 0.9899 | DNA_methylationHypermethylation of the hMLH1 promoter was observed in 6 ( 46 % ) of the 13 sporadic MSI - H tumors but not in any of the 3 hereditary MSI - H tumors or 13 MSI - L tumors. |
| 0.9869 | Hypermethylation of the hMLH1 Entitypromoter was observed in 6 ( 46 % ) of the 13 sporadic MSI - H tumors but not in any of the 3 hereditary MSI - H tumors or 13 MSI - L tumors. |
| 0.9686 | Hypermethylation of the ProteinhMLH1 promoter was observed in 6 ( 46 % ) of the 13 sporadic MSI - H tumors but not in any of the 3 hereditary MSI - H tumors or 13 MSI - L tumors. |
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|---|---|
| 0.9980 | All of the 3 HNPCC cases had germ - line ProteinhMLH1 mutation accompanied by loss of heterogeneity or other mutation in the tumor. |
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| 0.9994 | Our results also suggest the principal involvement of epigenetic or genetic inactivation of the ProteinhMLH1 gene in the pathogenesis of pancreatic carcinoma with MSI - H. |
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| 0.9931 | The acetylation state of human fetal hemoglobin modulates the strength of its subunit interactions : long - range effects and implications for Proteinhistone interactions in the nucleosome. |
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| 0.9895 | Evidence for this conclusion was obtained by demonstrating that natural hemoglobin F ( 1 ), which is specifically Acetylationacetylated at Gly - 1 ( gamma ) and hence unable to be protonated, behaves like HbA and not HbF in its tetramer - dimer association properties over the pH range studied. |
| 0.5746 | Evidence for this conclusion was obtained by demonstrating that natural hemoglobin F ( 1 ), which is specifically acetylated at Gly - 1 ( gamma ) and hence unable to be protonated, behaves like HbA and not ProteinHbF in its tetramer - dimer association properties over the pH range studied. |
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| 0.7990 | An increased degree of protonation of the gamma - chain N - terminus of Proteinhemoglobin F from pH 9. 0 to 8. 0 is therefore suggested as responsible for its increased tetramer strength representing an example of transmission of a signal from its positively charged N - terminal tail to the distant subunit allosteric interface where the equilibrium constant is measured. |
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| 0.9642 | An analogy is made between the effects of acetylation of the fetal hemoglobin tetramer on the strength of its subunit interactions and acetylation of some internal Lys residues within the N - terminal segments of the Proteinhistone octamer around which DNA is wrapped in the nucleosome. |
| 0.8934 | An analogy is made between the effects of acetylation of the fetal hemoglobin tetramer on the strength of its subunit interactions and Acetylationacetylation of some internal Lys residues within the N - terminal segments of the histone octamer around which DNA is wrapped in the nucleosome. |
| 0.8563 | An analogy is made between the effects of Acetylationacetylation of the fetal hemoglobin tetramer on the strength of its subunit interactions and acetylation of some internal Lys residues within the N - terminal segments of the histone octamer around which DNA is wrapped in the nucleosome. |
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| 0.9980 | Synergism of ProteinXist RNA, DNA methylation, and histone hypoacetylation in maintaining X chromosome inactivation. |
| 0.9979 | Synergism of Xist RNA, DNA methylation, and Proteinhistone hypoacetylation in maintaining X chromosome inactivation. |
| 0.9572 | Synergism of Xist RNA, DNA methylation, and histone Acetylationhypoacetylation in maintaining X chromosome inactivation. |
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| 0.9952 | ProteinXist RNA expression, methylation of CpG islands, and hypoacetylation of histone H4 are distinguishing features of inactive X chromatin. |
| 0.9492 | Xist RNA expression, methylation of CpG islands, and Acetylationhypoacetylation of histone H4 are distinguishing features of inactive X chromatin. |
| 0.9371 | Xist RNA expression, methylation of CpG islands, and hypoacetylation of Proteinhistone H4 are distinguishing features of inactive X chromatin. |
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| 0.9994 | ProteinXist RNA has been shown to be essential for initiation of X inactivation, but not required for maintenance. |
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| 0.9992 | Using a conditional mutant ProteinXist allele, we provide direct evidence for that loss of Xist RNA destabilizes the inactive state in somatic cells, leading to an increased reactivation frequency of an X - linked GFP transgene and of the endogenous hypoxanthine phosphoribosyl transferase ( Hprt ) gene in mouse embryonic fibroblasts. |
| 0.9990 | Using a conditional mutant Xist allele, we provide direct evidence for that loss of ProteinXist RNA destabilizes the inactive state in somatic cells, leading to an increased reactivation frequency of an X - linked GFP transgene and of the endogenous hypoxanthine phosphoribosyl transferase ( Hprt ) gene in mouse embryonic fibroblasts. |
| 0.9937 | Using a conditional mutant Xist allele, we provide direct evidence for that loss of Xist RNA destabilizes the inactive state in somatic cells, leading to an increased reactivation frequency of an X - linked ProteinGFP transgene and of the endogenous hypoxanthine phosphoribosyl transferase ( Hprt ) gene in mouse embryonic fibroblasts. |
| 0.9802 | Using a conditional mutant Xist allele, we provide direct evidence for that loss of Xist RNA destabilizes the inactive state in somatic cells, leading to an increased reactivation frequency of an X - linked GFP transgene and of the endogenous hypoxanthine phosphoribosyl transferase Protein( Hprt ) gene in mouse embryonic fibroblasts. |
| 0.7822 | Using a conditional mutant Xist allele, we provide direct evidence for that loss of Xist RNA destabilizes the inactive state in somatic cells, leading to an increased reactivation frequency of an X - linked GFP transgene and of the endogenous Proteinhypoxanthine phosphoribosyl transferase ( Hprt ) gene in mouse embryonic fibroblasts. |
| 0.6631 | Using a conditional mutant Xist allele, we provide direct evidence for that loss of Xist RNA destabilizes the inactive state in somatic cells, leading to an increased reactivation frequency of an X - linked GFP transgene and of the endogenous hypoxanthine Proteinphosphoribosyl transferase ( Hprt ) gene in mouse embryonic fibroblasts. |
| Score | Text |
|---|---|
| 0.9998 | Demethylation of DNA, using 5 - azadC or by introducing a mutation in ProteinDnmt1 , and inhibition of histone hypoacetylation using trichostatin A further increases reactivation in Xist mutant fibroblasts, indicating a synergistic interaction of X chromosome silencing mechanisms. |
| 0.9990 | Demethylation of DNA, using 5 - azadC or by introducing a mutation in Dnmt1, and inhibition of histone hypoacetylation using trichostatin A further increases reactivation in ProteinXist mutant fibroblasts, indicating a synergistic interaction of X chromosome silencing mechanisms. |
| 0.9982 | Demethylation of DNA, using 5 - azadC or by introducing a mutation in Dnmt1, and inhibition of Proteinhistone hypoacetylation using trichostatin A further increases reactivation in Xist mutant fibroblasts, indicating a synergistic interaction of X chromosome silencing mechanisms. |
| 0.9328 | Demethylation of DNA, using 5 - azadC or by introducing a mutation in Dnmt1, and inhibition of histone Acetylationhypoacetylation using trichostatin A further increases reactivation in Xist mutant fibroblasts, indicating a synergistic interaction of X chromosome silencing mechanisms. |
| Score | Text |
|---|---|
| 0.9876 | Expression of Pichia anomala ProteinINV1 gene in Saccharomyces cerevisiae results in two different active forms of hypoglycosylated invertase. |
| 0.9655 | Expression of Pichia anomala INV1 gene in Saccharomyces cerevisiae results in two different active forms of hypoglycosylated Proteininvertase . |
| 0.7915 | Expression of Pichia anomala INV1 gene in Saccharomyces cerevisiae results in two different active forms of Glycosylationhypoglycosylated invertase. |
| 0.3612 | Expression of Pichia anomala INV1 gene in Saccharomyces cerevisiae results in two different active forms of Glycosylationhypoglycosylated invertase . |
| Score | Text |
|---|---|
| 0.9959 | The Pichia anomala invertase gene Protein( INV1 ) was introduced at different copy numbers into a sucrose - nonfermenting mutant of Saccharomyces cerevisiae and expressed from its own promoter sequences. |
| 0.9814 | The Pichia anomala Proteininvertase gene ( INV1 ) was introduced at different copy numbers into a sucrose - nonfermenting mutant of Saccharomyces cerevisiae and expressed from its own promoter sequences. |
| Score | Text |
|---|---|
| 0.9998 | The level reached in the production of invertase by the transformants ( up to 540 units / 10 ( 10 ) cells ) was in agreement with the ProteinINV1 gene dosage. |
| 0.9996 | The level reached in the production of Proteininvertase by the transformants ( up to 540 units / 10 ( 10 ) cells ) was in agreement with the INV1 gene dosage. |
| Score | Text |
|---|---|
| 0.9991 | Two forms of multimeric active and glycosylated Proteininvertase displaying different subcellular locations and molecular masses could be detected in the transformants. |
| 0.9923 | Two forms of multimeric active and Glycosylationglycosylated invertase displaying different subcellular locations and molecular masses could be detected in the transformants. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9992 | Each of the two heterologous forms of Proteininvertase was shown to be an oligomer composed of identical subunits. |
| Score | Text |
|---|---|
| 0.9700 | The difference found in the apparent molecular masses of their monomers ( 81. 5 and 78. 3 kDa, respectively ) seems to be due to the size of their GlycosylationN - linked oligosaccharide chains ( on average 2. 4 and 1. 9 kDa, respectively ), since the number of sugar chains ( 9 ) and the molecular mass of the protein moiety ( 60. 5 kDa ) are identical in both forms. |
| 0.6540 | The difference found in the apparent molecular masses of their monomers ( 81. 5 and 78. 3 kDa, respectively ) seems to be due to the size of their N - linked Entityoligosaccharide chains ( on average 2. 4 and 1. 9 kDa, respectively ), since the number of sugar chains ( 9 ) and the molecular mass of the protein moiety ( 60. 5 kDa ) are identical in both forms. |
| 0.8428 | The difference found in the apparent molecular masses of their monomers ( 81. 5 and 78. 3 kDa, respectively ) seems to be due to the size of their N - linked Entityoligosaccharide chains ( on average 2. 4 and 1. 9 kDa, respectively ), since the number of sugar chains ( 9 ) and the molecular mass of the protein moiety ( 60. 5 kDa ) are identical in both forms. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9991 | The hypoglycosylated Proteininvertase accumulated within the cells of the transformants to an unusual level ( up to 130 units / 10 ( 10 ) cells ). |
| 0.9436 | The Glycosylationhypoglycosylated invertase accumulated within the cells of the transformants to an unusual level ( up to 130 units / 10 ( 10 ) cells ). |
| Score | Text |
|---|---|
| 0.9873 | Such accumulation of active enzyme inside the cells, as well as its underglycosylation, could be due to intrinsic properties of the P. anomala Proteininvertase that are determined by the particular primary structure of its protein moiety. |
| 0.8928 | Such accumulation of active enzyme inside the cells, as well as its Glycosylationunderglycosylation , could be due to intrinsic properties of the P. anomala invertase that are determined by the particular primary structure of its protein moiety. |
| Score | Text |
|---|---|
| 0.9989 | The histone acetyltransferase, ProteinhGCN5 , interacts with and acetylates the HIV transactivator, Tat. |
| 0.9973 | The histone acetyltransferase, hGCN5, interacts with and acetylates the HIV transactivator, ProteinTat . |
| 0.9253 | The Proteinhistone acetyltransferase, hGCN5, interacts with and acetylates the HIV transactivator, Tat. |
| 0.6166 | The histone acetyltransferase, hGCN5, interacts with and Acetylationacetylates the HIV transactivator, Tat. |
| The histone acetyltransferase, hGCN5, interacts with and Catalysisacetylates the HIV transactivator, Tat. | |
| Score | Text |
|---|---|
| 0.9885 | Factor acetyltransferase activity associated with several Proteinhistone acetyltransferases plays a key role in the control of transcription. |
| Score | Text |
|---|---|
| 0.9991 | Here we report that ProteinhGCN5 , a well known histone acetyltransferase, specifically interacts with and acetylates the human immunodeficiency virus type 1 ( HIV - 1 ) transactivator protein, Tat. |
| 0.9980 | Here we report that hGCN5, a well known histone acetyltransferase, specifically interacts with and acetylates the human immunodeficiency virus type 1 ( HIV - 1 ) transactivator protein, ProteinTat . |
| 0.9107 | Here we report that hGCN5, a well known Proteinhistone acetyltransferase, specifically interacts with and acetylates the human immunodeficiency virus type 1 ( HIV - 1 ) transactivator protein, Tat. |
| 0.6106 | Here we report that hGCN5, a well known histone acetyltransferase, specifically interacts with and Acetylationacetylates the human immunodeficiency virus type 1 ( HIV - 1 ) transactivator protein, Tat. |
| Here we report that hGCN5, a well known histone acetyltransferase, specifically interacts with and Catalysisacetylates the human immunodeficiency virus type 1 ( HIV - 1 ) transactivator protein, Tat. | |
| Score | Text |
|---|---|
| 0.9997 | The interaction between Tat and ProteinhGCN5 is direct and involves the acetyltransferase and the bromodomain regions of hGCN5, as well as a limited region of Tat encompassing the cysteine - rich domain of the protein. |
| 0.9997 | The interaction between Tat and hGCN5 is direct and involves the acetyltransferase and the bromodomain regions of ProteinhGCN5 , as well as a limited region of Tat encompassing the cysteine - rich domain of the protein. |
| 0.9996 | The interaction between ProteinTat and hGCN5 is direct and involves the acetyltransferase and the bromodomain regions of hGCN5, as well as a limited region of Tat encompassing the cysteine - rich domain of the protein. |
| 0.9996 | The interaction between Tat and hGCN5 is direct and involves the acetyltransferase and the bromodomain regions of hGCN5, as well as a limited region of ProteinTat encompassing the cysteine - rich domain of the protein. |
| Score | Text |
|---|---|
| 0.9948 | Tat lysines 50 and 51, target of acetylation by p300 / CBP, were also found to be acetylated by ProteinhGCN5 . |
| 0.9765 | Tat lysines 50 and 51, target of acetylation by Proteinp300 / CBP , were also found to be acetylated by hGCN5. |
| 0.9588 | ProteinTat lysines 50 and 51, target of acetylation by p300 / CBP, were also found to be acetylated by hGCN5. |
| 0.9549 | Tat lysines 50 and 51, target of Acetylationacetylation by p300 / CBP, were also found to be acetylated by hGCN5. |
| 0.9433 | Tat Entitylysines 50 and 51, target of acetylation by p300 / CBP, were also found to be acetylated by hGCN5. |
| 0.9246 | Tat lysines 50 and Entity51 , target of acetylation by p300 / CBP, were also found to be acetylated by hGCN5. |
| 0.7615 | Tat lysines 50 and 51, target of acetylation by p300 / CBP, were also found to be Acetylationacetylated by hGCN5. |
| 0.6654 | Tat Entitylysines 50 and 51, target of acetylation by p300 / CBP, were also found to be acetylated by hGCN5. |
| 0.5247 | Tat lysines Entity50 and 51, target of acetylation by p300 / CBP, were also found to be acetylated by hGCN5. |
| Tat lysines 50 and 51, target of acetylation by p300 / CBP, were also found to be Catalysisacetylated by hGCN5. | |
| Score | Text |
|---|---|
| 0.9970 | The acetylation of these two lysines by p300 / CBP has been recently shown to stimulate Tat transcriptional activity and accordingly, we have found that ProteinhGCN5 can considerably enhance Tat - dependent transcription of the HIV - 1 long terminal repeat. |
| 0.9952 | The acetylation of these two lysines by p300 / CBP has been recently shown to stimulate Tat transcriptional activity and accordingly, we have found that hGCN5 can considerably enhance ProteinTat - dependent transcription of the HIV - 1 long terminal repeat. |
| 0.9942 | The acetylation of these two lysines by Proteinp300 / CBP has been recently shown to stimulate Tat transcriptional activity and accordingly, we have found that hGCN5 can considerably enhance Tat - dependent transcription of the HIV - 1 long terminal repeat. |
| 0.9940 | The Acetylationacetylation of these two lysines by p300 / CBP has been recently shown to stimulate Tat transcriptional activity and accordingly, we have found that hGCN5 can considerably enhance Tat - dependent transcription of the HIV - 1 long terminal repeat. |
| 0.9935 | The acetylation of these two lysines by p300 / CBP has been recently shown to stimulate ProteinTat transcriptional activity and accordingly, we have found that hGCN5 can considerably enhance Tat - dependent transcription of the HIV - 1 long terminal repeat. |
| 0.9825 | The acetylation of these two Entitylysines by p300 / CBP has been recently shown to stimulate Tat transcriptional activity and accordingly, we have found that hGCN5 can considerably enhance Tat - dependent transcription of the HIV - 1 long terminal repeat. |
| Score | Text |
|---|---|
| 0.9933 | These data highlight the importance of the acetylation of lysines 50 and 51 in the function of Tat, since different histone acetyltransferases involved in distinct signaling pathways, ProteinGCN5 and p300 / CBP, converge to acetylate Tat on the same site. |
| 0.9855 | These data highlight the importance of the acetylation of lysines 50 and 51 in the function of ProteinTat , since different histone acetyltransferases involved in distinct signaling pathways, GCN5 and p300 / CBP, converge to acetylate Tat on the same site. |
| 0.9854 | These data highlight the importance of the Acetylationacetylation of lysines 50 and 51 in the function of Tat, since different histone acetyltransferases involved in distinct signaling pathways, GCN5 and p300 / CBP, converge to acetylate Tat on the same site. |
| 0.9808 | These data highlight the importance of the acetylation of lysines 50 and 51 in the function of Tat, since different histone acetyltransferases involved in distinct signaling pathways, GCN5 and Proteinp300 / CBP , converge to acetylate Tat on the same site. |
| 0.9730 | These data highlight the importance of the acetylation of lysines 50 and 51 in the function of Tat, since different Proteinhistone acetyltransferases involved in distinct signaling pathways, GCN5 and p300 / CBP, converge to acetylate Tat on the same site. |
| 0.9638 | These data highlight the importance of the acetylation of lysines 50 and 51 in the function of Tat, since different histone acetyltransferases involved in distinct signaling pathways, GCN5 and p300 / CBP, converge to acetylate ProteinTat on the same site. |
| 0.9603 | These data highlight the importance of the acetylation of Entitylysines 50 and 51 in the function of Tat, since different histone acetyltransferases involved in distinct signaling pathways, GCN5 and p300 / CBP, converge to acetylate Tat on the same site. |
| 0.9145 | These data highlight the importance of the acetylation of lysines 50 and Entity51 in the function of Tat, since different histone acetyltransferases involved in distinct signaling pathways, GCN5 and p300 / CBP, converge to acetylate Tat on the same site. |
| 0.6727 | These data highlight the importance of the acetylation of lysines 50 and 51 in the function of Tat, since different histone acetyltransferases involved in distinct signaling pathways, GCN5 and p300 / CBP, converge to Acetylationacetylate Tat on the same site. |
| 0.8143 | These data highlight the importance of the acetylation of Entitylysines 50 and 51 in the function of Tat, since different histone acetyltransferases involved in distinct signaling pathways, GCN5 and p300 / CBP, converge to acetylate Tat on the same site. |
| These data highlight the importance of the acetylation of lysines 50 and 51 in the function of Tat, since different histone acetyltransferases involved in distinct signaling pathways, GCN5 and p300 / CBP, converge to Catalysisacetylate Tat on the same site. | |
| Score | Text |
|---|---|
| 0.9858 | Hydroxylating activity of frog epidermis Proteintyrosinase . |
| Score | Text |
|---|---|
| 0.9951 | Trypsin activated in a similar way both the tyrosine hydroxylase and the dopa - oxidasa activities of frog epidermis Proteintyrosinase . |
| 0.9591 | Trypsin activated in a similar way both the Proteintyrosine hydroxylase and the dopa - oxidasa activities of frog epidermis tyrosinase. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9577 | ProteinTyrosine hydroxylase had KM = 2. 6 X 10 ( - 3 ) M for tyrosine and 2 x 10 ( - 3 ) M dopa was a competitive inhibitor with Ki = 5 x 10 ( - 4 ) M. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9957 | Canine ProteinCOL1A2 mutation resulting in C - terminal truncation of pro - alpha2 ( I ) and severe osteogenesis imperfecta. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9993 | In a nonisotopic RNAse cleavage assay ( NIRCA ), the proband's RNA had a unique cleavage pattern in the region of ProteinCOL1A2 encoding the C - propeptide. |
| 0.9987 | In a nonisotopic RNAse cleavage assay ( NIRCA ), the proband's RNA had a unique cleavage pattern in the region of COL1A2 encoding the ProteinC - propeptide . |
| Score | Text |
|---|---|
| 0.9901 | DNA sequence analyses identified a mutation in which nucleotides 3991 - 3994 ( " CTAG " ) were replaced with " TGTCATTGG. " The first seven bases of the inserted sequence were identical to nucleotides 4002 - 4008 of the normal canine ProteinCOL1A2 sequence. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9980 | Increased density of ProteinpC - alpha2 ( I ) suggested comigration with the similarly sized pro - alpha2 ( I ) derived from the mutant allele. |
| 0.9897 | Increased density of pC - alpha2 ( I ) suggested comigration with the similarly sized Proteinpro - alpha2 ( I ) derived from the mutant allele. |
| Score | Text |
|---|---|
| 0.9948 | Furthermore, a - chains were overhydroxylated and the ratio of Proteinalpha1 ( I ) : alpha2 ( I ) was 3. 2 : 1, consistent with the presence of alpha1 ( I ) homotrimers. |
| 0.9905 | Furthermore, a - chains were overhydroxylated and the ratio of alpha1 ( I ) : alpha2 ( I ) was 3. 2 : 1, consistent with the presence of Proteinalpha1 ( I ) homotrimers. |
| 0.2319 | Furthermore, a - chains were Hydroxylationoverhydroxylated and the ratio of alpha1 ( I ) : alpha2 ( I ) was 3. 2 : 1, consistent with the presence of alpha1 ( I ) homotrimers. |
| Score | Text |
|---|---|
| 0.9992 | Analyses of ProteinCOL1A2 and type I collagen were both consistent with the described heterozygous mutation affecting the pro - alpha2 ( I ) C - propeptide and confirmed a diagnosis of OI. |
| 0.9913 | Analyses of COL1A2 and type I collagen were both consistent with the described heterozygous mutation affecting the Proteinpro - alpha2 ( I ) C - propeptide and confirmed a diagnosis of OI. |
| Score | Text |
|---|---|
| 0.9969 | Linking global Proteinhistone acetylation to the transcription enhancement of X - chromosomal genes in Drosophila males. |
| 0.9966 | Linking global histone Acetylationacetylation to the transcription enhancement of X - chromosomal genes in Drosophila males. |
| Score | Text |
|---|---|
| 0.9966 | It has become well established for several genes that targeting of Proteinhistone acetylation to promoters is required for the activation of transcription. |
| 0.9949 | It has become well established for several genes that targeting of histone Acetylationacetylation to promoters is required for the activation of transcription. |
| Score | Text |
|---|---|
| 0.9376 | In contrast, global patterns of Acetylationacetylation have not been ascribed to any particular regulatory function. |
| Score | Text |
|---|---|
| 0.9982 | In Drosophila, a specific modification of ProteinH4 , acetylation at lysine 16, is enriched at hundreds of sites on the male X chromosome due to the activity of the male - specific lethal ( MSL ) dosage compensation complex. |
| 0.9936 | In Drosophila, a specific modification of H4, Acetylationacetylation at lysine 16, is enriched at hundreds of sites on the male X chromosome due to the activity of the male - specific lethal ( MSL ) dosage compensation complex. |
| 0.9415 | In Drosophila, a specific modification of H4, acetylation at Entitylysine 16 , is enriched at hundreds of sites on the male X chromosome due to the activity of the male - specific lethal ( MSL ) dosage compensation complex. |
| 0.5570 | In Drosophila, a specific modification of H4, acetylation at Entitylysine 16, is enriched at hundreds of sites on the male X chromosome due to the activity of the male - specific lethal ( MSL ) dosage compensation complex. |
| Score | Text |
|---|---|
| 0.9858 | Utilizing chromatin immunoprecipitation, we have determined that H4Ac16 is present along the entire length of X - linked genes targeted by the MSL complex with relatively modest levels of Acetylationacetylation at the promoter regions and high levels in the middle and / or 3'end of the transcription units. |
| 0.9683 | Utilizing chromatin immunoprecipitation, we have determined that ProteinH4Ac16 is present along the entire length of X - linked genes targeted by the MSL complex with relatively modest levels of acetylation at the promoter regions and high levels in the middle and / or 3'end of the transcription units. |
| Utilizing chromatin immunoprecipitation, we have determined that EntityH4Ac16 is present along the entire length of X - linked genes targeted by the MSL complex with relatively modest levels of acetylation at the promoter regions and high levels in the middle and / or 3'end of the transcription units. | |
| Score | Text |
|---|---|
| 0.9508 | We propose that global Acetylationacetylation by the MSL complex increases the expression of X - linked genes by facilitating transcription elongation rather than by enhancing promoter accessibility. |
| Score | Text |
|---|---|
| 0.9967 | We have also determined that ProteinH4Ac16 is absent from a region of the X chromosome that includes a gene known to be dosage - compensated by a MSL - independent mechanism. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9937 | Correlation between histone lysine methylation and developmental changes at the chicken Proteinbeta - globin locus. |
| 0.9655 | Correlation between Proteinhistone lysine methylation and developmental changes at the chicken beta - globin locus. |
| 0.9525 | Correlation between histone lysine Methylationmethylation and developmental changes at the chicken beta - globin locus. |
| 0.9095 | Correlation between histone Entitylysine methylation and developmental changes at the chicken beta - globin locus. |
| Score | Text |
|---|---|
| 0.9852 | Methylation of Proteinhistones at specific residues plays an important role in transcriptional regulation. |
| 0.9722 | MethylationMethylation of histones at specific residues plays an important role in transcriptional regulation. |
| Score | Text |
|---|---|
| 0.9962 | Chromatin immunoprecipitation of dimethylated lysine 9 on histone H3 across 53 kilobases of the chicken Proteinbeta - globin locus during erythropoiesis shows an almost complete anticorrelation between regions of elevated lysine 9 methylation and acetylation. |
| 0.9866 | Chromatin immunoprecipitation of dimethylated lysine 9 on histone H3 across 53 kilobases of the chicken beta - globin locus during erythropoiesis shows an almost complete anticorrelation between regions of elevated lysine 9 Methylationmethylation and acetylation. |
| 0.9472 | Chromatin immunoprecipitation of dimethylated lysine 9 on histone H3 across 53 kilobases of the chicken beta - globin locus during erythropoiesis shows an almost complete anticorrelation between regions of elevated Entitylysine 9 methylation and acetylation. |
| 0.8892 | Chromatin immunoprecipitation of dimethylated lysine 9 on histone H3 across 53 kilobases of the chicken beta - globin locus during erythropoiesis shows an almost complete anticorrelation between regions of elevated lysine 9 methylation and Acetylationacetylation . |
| 0.8396 | Chromatin immunoprecipitation of dimethylated lysine 9 on Proteinhistone H3 across 53 kilobases of the chicken beta - globin locus during erythropoiesis shows an almost complete anticorrelation between regions of elevated lysine 9 methylation and acetylation. |
| 0.7354 | Chromatin immunoprecipitation of Methylationdimethylated lysine 9 on histone H3 across 53 kilobases of the chicken beta - globin locus during erythropoiesis shows an almost complete anticorrelation between regions of elevated lysine 9 methylation and acetylation. |
| 0.7054 | Chromatin immunoprecipitation of dimethylated Entitylysine 9 on histone H3 across 53 kilobases of the chicken beta - globin locus during erythropoiesis shows an almost complete anticorrelation between regions of elevated lysine 9 methylation and acetylation. |
| 0.7563 | Chromatin immunoprecipitation of dimethylated lysine 9 on histone H3 across 53 kilobases of the chicken beta - globin locus during erythropoiesis shows an almost complete anticorrelation between regions of elevated Entitylysine 9 methylation and acetylation. |
| Score | Text |
|---|---|
| 0.9681 | Lysine 9 is Methylationmethylated most over constitutive condensed chromatin and developmentally inactive globin genes. |
| 0.8260 | EntityLysine 9 is methylated most over constitutive condensed chromatin and developmentally inactive globin genes. |
| Score | Text |
|---|---|
| 0.9724 | In contrast, lysine 4 methylation of histone H3 correlates with H3 Acetylationacetylation . |
| 0.9719 | In contrast, lysine 4 methylation of histone H3 correlates with ProteinH3 acetylation. |
| 0.9194 | In contrast, lysine 4 methylation of Proteinhistone H3 correlates with H3 acetylation. |
| 0.8455 | In contrast, lysine 4 Methylationmethylation of histone H3 correlates with H3 acetylation. |
| In contrast, Entitylysine 4 methylation of histone H3 correlates with H3 acetylation. | |
| Score | Text |
|---|---|
| 0.9923 | These results lead us to propose a mechanism by which the insulator in the Proteinbeta - globin locus can protect the globin genes from being silenced by adjacent condensed chromatin. |
| Score | Text |
|---|---|
| 0.9753 | Purification and characterization of a soluble bioactive amino - terminal extracellular domain of the human Proteinthyrotropin receptor . |
| Score | Text |
|---|---|
| 0.9469 | The amino - terminal ectodomain of the human ProteinTSH receptor has been expressed at the surface of CHO cells as a glycosylphosphatidylinositol - anchored molecule containing a 10 - residue histidine tag close to its C terminus. |
| 0.7491 | The amino - terminal ectodomain of the human TSH receptor has been expressed at the surface of CHO cells as a Glycosylationglycosylphosphatidylinositol - anchored molecule containing a 10 - residue histidine tag close to its C terminus. |
| The amino - terminal ectodomain of the human TSH receptor has been expressed at the surface of CHO cells as a Entityglycosylphosphatidylinositol - anchored molecule containing a 10 - residue histidine tag close to its C terminus. | |
| Score | Text |
|---|---|
| 0.8493 | The soluble ectodomain could be released from the cells by treatment with a Proteinglycosylphosphatidylinositol - phospholipase C and purified to apparent homogeneity by cobalt - Sepharose chromatography. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9916 | This allowed the identification of four out of the six potential N - glycosylation sites as being effectively Glycosylationglycosylated . |
| 0.7807 | This allowed the identification of four out of the six potential EntityN - glycosylation sites as being effectively glycosylated. |
| 0.6101 | This allowed the identification of four out of the six potential EntityN - glycosylation sites as being effectively glycosylated. |
| Score | Text |
|---|---|
| 0.9913 | A proportion of the purified soluble ectodomain displayed specific binding of ( 125 ) I - labeled ProteinTSH , allowing for the first time performance of classical saturation binding experiments. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9976 | Contrary to all currently available assays, the soluble ectodomain of the TSH receptor purified in a functionally competent conformation allows direct studies of its interactions with ProteinTSH and autoantibodies and opens the way to structural studies. |
| 0.9790 | Contrary to all currently available assays, the soluble ectodomain of the ProteinTSH receptor purified in a functionally competent conformation allows direct studies of its interactions with TSH and autoantibodies and opens the way to structural studies. |
| Score | Text |
|---|---|
| 0.9988 | ProteinHIF - 1alpha binding to VHL is regulated by stimulus - sensitive proline hydroxylation. |
| 0.9982 | HIF - 1alpha binding to ProteinVHL is regulated by stimulus - sensitive proline hydroxylation. |
| 0.9823 | HIF - 1alpha binding to VHL is regulated by stimulus - sensitive Entityproline hydroxylation. |
| 0.9502 | HIF - 1alpha binding to VHL is regulated by stimulus - sensitive proline Hydroxylationhydroxylation . |
| Score | Text |
|---|---|
| 0.9507 | Hypoxia - inducible factor - 1alpha Protein( HIF - 1alpha ) is a global transcriptional regulator of the hypoxic response. |
| 0.7768 | ProteinHypoxia - inducible factor - 1alpha ( HIF - 1alpha ) is a global transcriptional regulator of the hypoxic response. |
| Score | Text |
|---|---|
| 0.9971 | Under normoxic conditions, ProteinHIF - 1alpha is recognized by the von Hippel - Lindau tumor - suppressor protein ( VHL ), a component of an E3 ubiquitin ligase complex. |
| 0.9899 | Under normoxic conditions, HIF - 1alpha is recognized by the von Hippel - Lindau tumor - suppressor protein ( VHL ), a component of an E3 Proteinubiquitin ligase complex. |
| 0.9859 | Under normoxic conditions, HIF - 1alpha is recognized by the von Hippel - Lindau tumor - suppressor protein Protein( VHL ) , a component of an E3 ubiquitin ligase complex. |
| 0.7529 | Under normoxic conditions, HIF - 1alpha is recognized by the Proteinvon Hippel - Lindau tumor - suppressor protein ( VHL ), a component of an E3 ubiquitin ligase complex. |
| 0.5662 | Under normoxic conditions, HIF - 1alpha is recognized by the von ProteinHippel - Lindau tumor - suppressor protein ( VHL ), a component of an E3 ubiquitin ligase complex. |
| Score | Text |
|---|---|
| 0.9990 | This interaction thereby promotes the rapid degradation of ProteinHIF - 1alpha . |
| Score | Text |
|---|---|
| 0.9985 | Under hypoxic conditions, ProteinHIF - 1alpha is stabilized. |
| Score | Text |
|---|---|
| 0.9994 | We have previously shown that ProteinVHL binds in a hypoxia - sensitive manner to a 27 - aa segment of HIF - 1alpha, and that this regulation depends on a posttranslational modification of HIF - 1alpha. |
| 0.9988 | We have previously shown that VHL binds in a hypoxia - sensitive manner to a 27 - aa segment of HIF - 1alpha, and that this regulation depends on a posttranslational modification of ProteinHIF - 1alpha . |
| 0.9987 | We have previously shown that VHL binds in a hypoxia - sensitive manner to a 27 - aa segment of ProteinHIF - 1alpha , and that this regulation depends on a posttranslational modification of HIF - 1alpha. |
| Score | Text |
|---|---|
| 0.9974 | Through a combination of in vivo coimmunoprecipitation assays using ProteinVHL and a panel of point mutants of HIF - 1alpha in this region, as well as MS and in vitro binding assays, we now provide evidence that this modification, which occurs under normoxic conditions, is hydroxylation of Pro - 564 of HIF - 1alpha. |
| 0.9960 | Through a combination of in vivo coimmunoprecipitation assays using VHL and a panel of point mutants of ProteinHIF - 1alpha in this region, as well as MS and in vitro binding assays, we now provide evidence that this modification, which occurs under normoxic conditions, is hydroxylation of Pro - 564 of HIF - 1alpha. |
| 0.9951 | Through a combination of in vivo coimmunoprecipitation assays using VHL and a panel of point mutants of HIF - 1alpha in this region, as well as MS and in vitro binding assays, we now provide evidence that this modification, which occurs under normoxic conditions, is hydroxylation of Pro - 564 of ProteinHIF - 1alpha . |
| 0.9949 | Through a combination of in vivo coimmunoprecipitation assays using VHL and a panel of point mutants of HIF - 1alpha in this region, as well as MS and in vitro binding assays, we now provide evidence that this modification, which occurs under normoxic conditions, is hydroxylation of EntityPro - 564 of HIF - 1alpha. |
| 0.9673 | Through a combination of in vivo coimmunoprecipitation assays using VHL and a panel of point mutants of HIF - 1alpha in this region, as well as MS and in vitro binding assays, we now provide evidence that this modification, which occurs under normoxic conditions, is Hydroxylationhydroxylation of Pro - 564 of HIF - 1alpha. |
| Score | Text |
|---|---|
| 0.9959 | The data furthermore show that this proline hydroxylation is the primary regulator of ProteinVHL binding. |
| Score | Text |
|---|---|
| 0.9992 | 2B4 ( CD244 ) and CS1 : novel members of the ProteinCD2 subset of the immunoglobulin superfamily molecules expressed on natural killer cells and other leukocytes. |
| 0.9981 | 2B4 ( CD244 ) and ProteinCS1 : novel members of the CD2 subset of the immunoglobulin superfamily molecules expressed on natural killer cells and other leukocytes. |
| 0.9837 | Protein2B4 ( CD244 ) and CS1 : novel members of the CD2 subset of the immunoglobulin superfamily molecules expressed on natural killer cells and other leukocytes. |
| 0.8892 | 2B4 Protein( CD244 ) and CS1 : novel members of the CD2 subset of the immunoglobulin superfamily molecules expressed on natural killer cells and other leukocytes. |
| 0.6130 | Protein2B4 ( CD244 ) and CS1 : novel members of the CD2 subset of the immunoglobulin superfamily molecules expressed on natural killer cells and other leukocytes. |
| Score | Text |
|---|---|
| 0.9994 | Protein2B4 is a member of the CD2 subset of the immunoglobulin superfamily molecules expressed on natural killer ( NK ) cells and other leukocytes. |
| 0.9990 | 2B4 is a member of the ProteinCD2 subset of the immunoglobulin superfamily molecules expressed on natural killer ( NK ) cells and other leukocytes. |
| Score | Text |
|---|---|
| 0.9989 | It is the high affinity ligand for ProteinCD48 . |
| Score | Text |
|---|---|
| 0.9989 | Engagement of 2B4 on NK - cell surfaces with specific antibodies or ProteinCD48 can trigger cell - mediated cytotoxicity, interferon - gamma secretion, phosphoinositol turnover and NK - cell invasiveness. |
| 0.9989 | Engagement of Protein2B4 on NK - cell surfaces with specific antibodies or CD48 can trigger cell - mediated cytotoxicity, interferon - gamma secretion, phosphoinositol turnover and NK - cell invasiveness. |
| 0.9979 | Engagement of 2B4 on NK - cell surfaces with specific antibodies or CD48 can trigger cell - mediated cytotoxicity, Proteininterferon - gamma secretion, phosphoinositol turnover and NK - cell invasiveness. |
| Score | Text |
|---|---|
| 0.9997 | The function of 2B4 in ProteinCD8 + T cells and myeloid cells remains unknown. |
| 0.9988 | The function of Protein2B4 in CD8 + T cells and myeloid cells remains unknown. |
| Score | Text |
|---|---|
| 0.9992 | The cytoplasmic domain of Protein2B4 contains unique tyrosine motifs ( TxYxxV / I ) that associate with src homology 2 domain - containing protein or signaling lymphocyte activation molecule ( SLAM ) - associated protein, whose mutation is the underlying genetic defect in the X - linked lymphoproliferative disease ( XLPD ). |
| 0.6419 | The cytoplasmic domain of 2B4 contains unique tyrosine motifs ( TxYxxV / I ) that associate with Proteinsrc homology 2 domain - containing protein or signaling lymphocyte activation molecule ( SLAM ) - associated protein, whose mutation is the underlying genetic defect in the X - linked lymphoproliferative disease ( XLPD ). |
| The cytoplasmic domain of 2B4 contains unique tyrosine motifs ( TxYxxV / I ) that associate with src homology 2 domain - containing protein or Proteinsignaling lymphocyte activation molecule ( SLAM ) - associated protein , whose mutation is the underlying genetic defect in the X - linked lymphoproliferative disease ( XLPD ). | |
| Score | Text |
|---|---|
| 0.9798 | Impaired signaling via Protein2B4 and SLAM is implicated in the immunopathogenesis of XLPD. |
| Score | Text |
|---|---|
| 0.9996 | CS1 is a novel member of the ProteinCD2 subset that contains two of the unique tyrosine motifs present in 2B4 and SLAM. |
| 0.9994 | ProteinCS1 is a novel member of the CD2 subset that contains two of the unique tyrosine motifs present in 2B4 and SLAM. |
| 0.9895 | CS1 is a novel member of the CD2 subset that contains two of the unique tyrosine motifs present in Protein2B4 and SLAM. |
| Score | Text |
|---|---|
| 0.9995 | Signaling through 2B4, CS1 and other members of the ProteinCD2 subset may play a major role in the regulation of NK cells and other leukocyte functions. |
| 0.9994 | Signaling through 2B4, ProteinCS1 and other members of the CD2 subset may play a major role in the regulation of NK cells and other leukocyte functions. |
| 0.9982 | Signaling through Protein2B4 , CS1 and other members of the CD2 subset may play a major role in the regulation of NK cells and other leukocyte functions. |
| Score | Text |
|---|---|
| 0.9840 | GlycosylationN - glycosylation of CRF receptor type 1 is important for its ligand - specific interaction. |
| 0.8376 | N - glycosylation of ProteinCRF receptor type 1 is important for its ligand - specific interaction. |
| Score | Text |
|---|---|
| 0.9446 | The corticotropin - releasing factor ( CRF ) receptor type 1 Protein( CRFR1 ) contains five potential N - glycosylation sites : N38, N45, N78, N90, and N98. |
| The Proteincorticotropin - releasing factor ( CRF ) receptor type 1 ( CRFR1 ) contains five potential N - glycosylation sites : N38, N45, N78, N90, and N98. | |
| Score | Text |
|---|---|
| 0.9994 | Cells expressing ProteinCRFR1 were treated with tunicamycin to block receptor glycosylation. |
| Score | Text |
|---|---|
| 0.9989 | The nonglycosylated receptor did not bind the radioligand and had a decreased cAMP stimulation potency in response to ProteinCRF . |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9935 | The single mutants Q38, Q45, Q78, Q90, Q98, A40, A47, A80, A92, and A100 and the double mutants A40 / A47 and A80 / A100 were well expressed, bound ProteinCRF , sauvagine ( SVG ), and urotensin - I ( UTS - I ) with a normal affinity, and increased cAMP accumulation with a high efficiency. |
| 0.9903 | The single mutants Q38, Q45, Q78, Q90, Q98, A40, A47, A80, A92, and A100 and the double mutants A40 / A47 and A80 / A100 were well expressed, bound CRF, sauvagine ( SVG ), and Proteinurotensin - I ( UTS - I ) with a normal affinity, and increased cAMP accumulation with a high efficiency. |
| 0.9861 | The single mutants Q38, Q45, Q78, Q90, Q98, A40, A47, A80, A92, and A100 and the double mutants A40 / A47 and A80 / A100 were well expressed, bound CRF, sauvagine ( SVG ), and urotensin - I Protein( UTS - I ) with a normal affinity, and increased cAMP accumulation with a high efficiency. |
| 0.9698 | The single mutants Q38, Q45, Q78, Q90, Q98, A40, A47, A80, A92, and A100 and the double mutants A40 / A47 and A80 / A100 were well expressed, bound CRF, sauvagine Protein( SVG ) , and urotensin - I ( UTS - I ) with a normal affinity, and increased cAMP accumulation with a high efficiency. |
| 0.9151 | The single mutants Q38, Q45, Q78, Q90, Q98, A40, A47, A80, A92, and A100 and the double mutants A40 / A47 and A80 / A100 were well expressed, bound CRF, Proteinsauvagine ( SVG ), and urotensin - I ( UTS - I ) with a normal affinity, and increased cAMP accumulation with a high efficiency. |
| 0.6232 | The single mutants Q38, Q45, Q78, Q90, Q98, A40, A47, A80, A92, and A100 and the double mutants A40 / A47 and A80 / A100 were well expressed, bound CRF, sauvagine ( SVG ), and Proteinurotensin - I ( UTS - I ) with a normal affinity, and increased cAMP accumulation with a high efficiency. |
| 0.6147 | The single mutants Q38, Q45, Q78, Q90, Q98, A40, A47, A80, A92, and A100 and the double mutants A40 / A47 and A80 / A100 were well expressed, bound CRF, Proteinsauvagine ( SVG ) , and urotensin - I ( UTS - I ) with a normal affinity, and increased cAMP accumulation with a high efficiency. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9998 | These data indicate the requirement for three or more polysaccharide chains for normal ProteinCRFR1 function. |
| Score | Text |
|---|---|
| 0.9998 | Reduced rates of gene loss, gene silencing, and gene mutation in ProteinDnmt1 - deficient embryonic stem cells. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9998 | In addition, we targeted the major DNA methyltransferase gene, ProteinDnmt1 , to investigate the relative contribution of DNA methylation to these various competing gene inactivation pathways. |
| Score | Text |
|---|---|
| 0.9993 | Our data show that gene loss is the predominant mode of inactivation of a herpes simplex virus thymidine kinase neomycin phosphotransferase reporter gene ( HSV - TKNeo ) at the two integration sites tested and that this event is significantly reduced in ProteinDnmt1 - deficient cells. |
| 0.5653 | Our data show that gene loss is the predominant mode of inactivation of a herpes simplex virus Proteinthymidine kinase neomycin phosphotransferase reporter gene ( HSV - TKNeo ) at the two integration sites tested and that this event is significantly reduced in Dnmt1 - deficient cells. |
| Score | Text |
|---|---|
| 0.9998 | Gene silencing by promoter methylation requires ProteinDnmt1 , suggesting that the expression of Dnmt3a and Dnmt3b alone in ES cells is insufficient to achieve effective gene silencing. |
| 0.9997 | Gene silencing by promoter methylation requires Dnmt1, suggesting that the expression of ProteinDnmt3a and Dnmt3b alone in ES cells is insufficient to achieve effective gene silencing. |
| 0.9997 | Gene silencing by promoter methylation requires Dnmt1, suggesting that the expression of Dnmt3a and ProteinDnmt3b alone in ES cells is insufficient to achieve effective gene silencing. |
| Score | Text |
|---|---|
| 0.9998 | We used a novel assay to show that missense mutation rates are also substantially reduced in ProteinDnmt1 - deficient cells. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9996 | Surprisingly, the fraction of CpG transition mutations was not reduced in ProteinDnmt1 - deficient cells. |
| Score | Text |
|---|---|
| 0.9997 | Finally, we show that methyl group - deficient growth conditions do not cause an increase in missense mutation rates in ProteinDnmt1 - proficient cells, as predicted by methyltransferase - mediated mutagenesis models. |
| Score | Text |
|---|---|
| 0.9999 | We conclude that ProteinDnmt1 deficiency and the accompanying genomic DNA hypomethylation result in a reduction of three major pathways of gene inactivation in our model system. |
| Score | Text |
|---|---|
| 0.9987 | Induction of hepatitis C virus ProteinE1 envelope protein - specific immune response can be enhanced by mutation of N - glycosylation sites. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9986 | We investigated the role played by N - glycans in the immunogenicity of hepatitis C virus ( HCV ) ProteinE1 envelope glycoprotein, a naturally poor immunogen. |
| Score | Text |
|---|---|
| 0.9996 | Eight plasmids were engineered, encoding ProteinE1 protein mutants in which the four N - linked glycosylation sites of the protein were mutated separately or in combination. |
| Score | Text |
|---|---|
| 0.6787 | In vitro expression studies showed an influence of GlycosylationN - linked glycosylation on expression efficiency, instability, and / or secretion of the mutated proteins. |
| 0.7581 | In vitro expression studies showed an influence of N - linked Glycosylationglycosylation on expression efficiency, instability, and / or secretion of the mutated proteins. |
| Score | Text |
|---|---|
| 0.9995 | Immunogenicity of the ProteinE1 mutants was studied in BALB / c mice following intramuscular and intraepidermal injection of the plasmids. |
| Score | Text |
|---|---|
| 0.9989 | Whereas some mutations had no or only minor effects on the antibody titers induced, mutation of the fourth glycosylation site ( N4 ) significantly enhanced the Proteinanti - E1 humoral response in terms of both seroconversion rates and antibody titers. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9996 | Epitope mapping indicated that the ProteinE1 mutant antigens induced antibody directed at two major domains : one, located at amino acids ( aa ) 313 to 332, which is known to be reactive with sera from HCV patients, and a second one, located in the N - terminal domain of E1 ( aa 192 to 226 ). |
| 0.9969 | Epitope mapping indicated that the E1 mutant antigens induced antibody directed at two major domains : one, located at amino acids ( aa ) 313 to 332, which is known to be reactive with sera from HCV patients, and a second one, located in the N - terminal domain of ProteinE1 ( aa 192 to 226 ). |
| Score | Text |
|---|---|
| 0.9356 | Analysis of the induced immune cellular response confirmed the induction of Proteingamma interferon - producing cells by all mutants, albeit to different levels. |
| 0.7378 | Analysis of the induced immune cellular response confirmed the induction of gamma Proteininterferon - producing cells by all mutants, albeit to different levels. |
| Score | Text |
|---|---|
| 0.9993 | These results show that N - linked glycosylation can limit the antibody response to the HCV ProteinE1 protein and reveal a potential vaccine candidate with enhanced immunogenicity. |
| 0.9191 | These results show that GlycosylationN - linked glycosylation can limit the antibody response to the HCV E1 protein and reveal a potential vaccine candidate with enhanced immunogenicity. |
| 0.9275 | These results show that N - linked Glycosylationglycosylation can limit the antibody response to the HCV E1 protein and reveal a potential vaccine candidate with enhanced immunogenicity. |
| 0.7148 | These results show that GlycosylationN - linked glycosylation can limit the antibody response to the HCV E1 protein and reveal a potential vaccine candidate with enhanced immunogenicity. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9993 | The BAH genomic locus encodes three distinct proteins : Proteinjunctin , humbug, and BAH. |
| 0.9993 | The BAH genomic locus encodes three distinct proteins : junctin, humbug, and ProteinBAH . |
| 0.9988 | The ProteinBAH genomic locus encodes three distinct proteins : junctin, humbug, and BAH. |
| 0.9987 | The BAH genomic locus encodes three distinct proteins : junctin, Proteinhumbug , and BAH. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9995 | The biological roles of ProteinBAH and humbug and their functional relationship to junctin remain unclear. |
| 0.9990 | The biological roles of BAH and humbug and their functional relationship to Proteinjunctin remain unclear. |
| 0.9990 | The biological roles of BAH and Proteinhumbug and their functional relationship to junctin remain unclear. |
| Score | Text |
|---|---|
| 0.9996 | To evaluate the role of ProteinBAH in vivo, the catalytic domain of BAH was specifically targeted such that the coding regions of junctin and humbug remained undisturbed. |
| 0.9995 | To evaluate the role of BAH in vivo, the catalytic domain of ProteinBAH was specifically targeted such that the coding regions of junctin and humbug remained undisturbed. |
| 0.9993 | To evaluate the role of BAH in vivo, the catalytic domain of BAH was specifically targeted such that the coding regions of junctin and Proteinhumbug remained undisturbed. |
| 0.9990 | To evaluate the role of BAH in vivo, the catalytic domain of BAH was specifically targeted such that the coding regions of Proteinjunctin and humbug remained undisturbed. |
| Score | Text |
|---|---|
| 0.9816 | BAH null mice lack measurable ProteinBAH protein in several tissues, lack aspartyl beta - hydroxylase activity in liver preparations, and exhibit no hydroxylation of the epidermal growth factor ( EGF ) domain of clotting Factor X. |
| 0.9787 | ProteinBAH null mice lack measurable BAH protein in several tissues, lack aspartyl beta - hydroxylase activity in liver preparations, and exhibit no hydroxylation of the epidermal growth factor ( EGF ) domain of clotting Factor X. |
| 0.9504 | BAH null mice lack measurable BAH protein in several tissues, lack aspartyl beta - hydroxylase activity in liver preparations, and exhibit no Hydroxylationhydroxylation of the epidermal growth factor ( EGF ) domain of clotting Factor X. |
| 0.9359 | BAH null mice lack measurable BAH protein in several tissues, lack aspartyl beta - hydroxylase activity in liver preparations, and exhibit no hydroxylation of the epidermal growth factor ( EGF ) domain of clotting ProteinFactor X . |
| 0.6169 | BAH null mice lack measurable BAH protein in several tissues, lack Proteinaspartyl beta - hydroxylase activity in liver preparations, and exhibit no hydroxylation of the epidermal growth factor ( EGF ) domain of clotting Factor X. |
| BAH null mice lack measurable BAH protein in several tissues, lack aspartyl beta - hydroxylase activity in liver preparations, and exhibit no hydroxylation of the Entityepidermal growth factor ( EGF ) domain of clotting Factor X. | |
| Score | Text |
|---|---|
| 0.9995 | In addition to reduced fertility in females, ProteinBAH null mice display several developmental defects including syndactyly, facial dysmorphology, and a mild defect in hard palate formation. |
| Score | Text |
|---|---|
| 0.9982 | The developmental defects present in ProteinBAH null mice are similar to defects observed in knock - outs and hypomorphs of the Notch ligand Serrate - 2. |
| 0.9975 | The developmental defects present in BAH null mice are similar to defects observed in knock - outs and hypomorphs of the Notch ligand ProteinSerrate - 2 . |
| Score | Text |
|---|---|
| 0.9909 | In this work, beta - hydroxylation of Asp residues in EGF domains is demonstrated for a soluble form of a Notch ligand, human ProteinJagged - 1 . |
| 0.9170 | In this work, Hydroxylationbeta - hydroxylation of Asp residues in EGF domains is demonstrated for a soluble form of a Notch ligand, human Jagged - 1. |
| 0.8369 | In this work, beta - hydroxylation of EntityAsp residues in EGF domains is demonstrated for a soluble form of a Notch ligand, human Jagged - 1. |
| 0.5882 | In this work, beta - hydroxylation of EntityAsp residues in EGF domains is demonstrated for a soluble form of a Notch ligand, human Jagged - 1. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9990 | Previous work has demonstrated increased levels of ProteinBAH in certain tumor tissues and a role for BAH in tumorigenesis has been proposed. |
| 0.9985 | Previous work has demonstrated increased levels of BAH in certain tumor tissues and a role for ProteinBAH in tumorigenesis has been proposed. |
| Score | Text |
|---|---|
| 0.9690 | The role of hydroxylase in tumor formation was tested directly by crossing ProteinBAH KO mice with an intestinal tumor model, APCmin mice. |
| Score | Text |
|---|---|
| 0.9996 | Surprisingly, ProteinBAH null / APCmin mice show a statistically significant increase in both intestinal polyp size and number when compared with BAH wild - type / APCmin controls. |
| 0.9988 | Surprisingly, BAH null / APCmin mice show a statistically significant increase in both intestinal polyp size and number when compared with ProteinBAH wild - type / APCmin controls. |
| Score | Text |
|---|---|
| 0.9989 | These results suggest that, in contrast to expectations, loss of ProteinBAH catalytic activity may promote tumor formation. |
| Score | Text |
|---|---|
| 0.9986 | Molecular cloning of ProteinESET , a novel histone H3 - specific methyltransferase that interacts with ERG transcription factor. |
| 0.9966 | Molecular cloning of ESET, a novel histone H3 - specific methyltransferase that interacts with ProteinERG transcription factor. |
| 0.9323 | Molecular cloning of ESET, a novel Proteinhistone H3 - specific methyltransferase that interacts with ERG transcription factor. |
| Score | Text |
|---|---|
| 0.9999 | The ets - related gene Proteinerg encodes a transcription factor that is implicated in the control of cell growth and differentiation. |
| Score | Text |
|---|---|
| 0.9998 | To identify interacting partners of ERG, we screened a yeast two - hybrid cDNA library constructed from mouse hematopoietic cells using the N - terminal region of ProteinERG as a bait. |
| 0.9998 | To identify interacting partners of ProteinERG , we screened a yeast two - hybrid cDNA library constructed from mouse hematopoietic cells using the N - terminal region of ERG as a bait. |
| Score | Text |
|---|---|
| 0.9931 | We isolated a 4. 6 kb full - length mouse cDNA encoding a 1307 - amino acid protein migrating as a 180 kD band, which was termed ProteinESET ( ERG - associated protein with SET domain ). |
| We isolated a 4. 6 kb full - length mouse cDNA encoding a 1307 - amino acid protein migrating as a 180 kD band, which was termed ESET Protein( ERG - associated protein with SET domain ) . | |
| Score | Text |
|---|---|
| 0.9991 | ProteinESET is 92 % identical to the human protein SETDB1 ( SET domain, bifurcated 1 ). |
| 0.9771 | ESET is 92 % identical to the human protein ProteinSETDB1 ( SET domain, bifurcated 1 ). |
| ESET is 92 % identical to the human protein SETDB1 Protein( SET domain, bifurcated 1 ) . | |
| Score | Text |
|---|---|
| 0.9998 | The interaction between ESET and ERG was supported by in vitro pull - down using glutathione S - transferase ( GST ) fusion protein, by transfection and co - immunoprecipitation experiments, and by association of endogenous ProteinSETDB1 with ERG. |
| 0.9998 | The interaction between ESET and ProteinERG was supported by in vitro pull - down using glutathione S - transferase ( GST ) fusion protein, by transfection and co - immunoprecipitation experiments, and by association of endogenous SETDB1 with ERG. |
| 0.9998 | The interaction between ESET and ERG was supported by in vitro pull - down using glutathione S - transferase ( GST ) fusion protein, by transfection and co - immunoprecipitation experiments, and by association of endogenous SETDB1 with ProteinERG . |
| 0.9997 | The interaction between ProteinESET and ERG was supported by in vitro pull - down using glutathione S - transferase ( GST ) fusion protein, by transfection and co - immunoprecipitation experiments, and by association of endogenous SETDB1 with ERG. |
| 0.6251 | The interaction between ESET and ERG was supported by in vitro pull - down using Proteinglutathione S - transferase ( GST ) fusion protein, by transfection and co - immunoprecipitation experiments, and by association of endogenous SETDB1 with ERG. |
| Score | Text |
|---|---|
| 0.9988 | Since ProteinESET possesses evolutionarily conserved SET, preSET, and postSET domains implicated in histone methylation, we tested the ability of ESET to methylate core histones. |
| 0.9986 | Since ESET possesses evolutionarily conserved SET, preSET, and postSET domains implicated in histone methylation, we tested the ability of ProteinESET to methylate core histones. |
| 0.9815 | Since ESET possesses evolutionarily conserved SET, preSET, and postSET domains implicated in histone methylation, we tested the ability of ESET to methylate core Proteinhistones . |
| 0.9770 | Since ESET possesses evolutionarily conserved SET, preSET, and postSET domains implicated in Proteinhistone methylation, we tested the ability of ESET to methylate core histones. |
| 0.9692 | Since ESET possesses evolutionarily conserved SET, preSET, and postSET domains implicated in histone Methylationmethylation , we tested the ability of ESET to methylate core histones. |
| 0.8421 | Since ESET possesses evolutionarily conserved SET, preSET, and postSET domains implicated in histone methylation, we tested the ability of ESET to Methylationmethylate core histones. |
| Score | Text |
|---|---|
| 0.9994 | The results of these studies demonstrated that ProteinESET is a histone H3 - specific methyltransferase, and that mutations within ESET abolished its methyltransferase activity. |
| 0.9993 | The results of these studies demonstrated that ESET is a histone H3 - specific methyltransferase, and that mutations within ProteinESET abolished its methyltransferase activity. |
| 0.9535 | The results of these studies demonstrated that ESET is a Proteinhistone H3 - specific methyltransferase, and that mutations within ESET abolished its methyltransferase activity. |
| Score | Text |
|---|---|
| 0.9992 | Together, these findings raise the possibility that transcription factor ProteinERG may participate in transcriptional regulation through ESET - mediated histone methylation. |
| 0.9505 | Together, these findings raise the possibility that transcription factor ERG may participate in transcriptional regulation through ESET - mediated histone Methylationmethylation . |
| 0.6013 | Together, these findings raise the possibility that transcription factor ERG may participate in transcriptional regulation through ProteinESET - mediated histone methylation. |
| 0.4680 | Together, these findings raise the possibility that transcription factor ERG may participate in transcriptional regulation through ProteinESET - mediated histone methylation. |
| Together, these findings raise the possibility that transcription factor ERG may participate in transcriptional regulation through ESET - mediated Proteinhistone methylation. | |
| Together, these findings raise the possibility that transcription factor ERG may participate in transcriptional regulation through CatalysisESET - mediated histone methylation. | |
| Score | Text |
|---|---|
| 0.8033 | Regulation of HIF by the Proteinvon Hippel - Lindau tumour suppressor : implications for cellular oxygen sensing. |
| 0.5814 | Regulation of HIF by the von ProteinHippel - Lindau tumour suppressor : implications for cellular oxygen sensing. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9990 | A key insight has been the recognition that HIF - alpha is targeted for degradation by the Proteinubiquitin - proteasome pathway through binding to the von Hippel - Lindau tumour suppressor protein ( pVHL ), which forms the recognition component of an E3 ubiquitin ligase complex leading to ubiquitylation of HIF - alpha. |
| 0.9953 | A key insight has been the recognition that HIF - alpha is targeted for degradation by the ubiquitin - proteasome pathway through binding to the von Hippel - Lindau tumour suppressor protein ( pVHL ), which forms the recognition component of an E3 Proteinubiquitin ligase complex leading to ubiquitylation of HIF - alpha. |
| 0.9911 | A key insight has been the recognition that HIF - alpha is targeted for degradation by the ubiquitin - proteasome pathway through binding to the von Hippel - Lindau tumour suppressor protein Protein( pVHL ) , which forms the recognition component of an E3 ubiquitin ligase complex leading to ubiquitylation of HIF - alpha. |
| 0.8337 | A key insight has been the recognition that HIF - alpha is targeted for degradation by the ubiquitin - proteasome pathway through binding to the Proteinvon Hippel - Lindau tumour suppressor protein ( pVHL ), which forms the recognition component of an E3 ubiquitin ligase complex leading to ubiquitylation of HIF - alpha. |
| 0.9391 | A key insight has been the recognition that HIF - alpha is targeted for degradation by the ubiquitin - proteasome pathway through binding to the von Hippel - Lindau tumour suppressor protein ( pVHL ), which forms the recognition component of an E3 ubiquitin ligase complex leading to Ubiquitinationubiquitylation of HIF - alpha. |
| 0.6917 | A key insight has been the recognition that HIF - alpha is targeted for degradation by the ubiquitin - proteasome pathway through binding to the von ProteinHippel - Lindau tumour suppressor protein ( pVHL ), which forms the recognition component of an E3 ubiquitin ligase complex leading to ubiquitylation of HIF - alpha. |
| Score | Text |
|---|---|
| 0.9892 | Importantly, the classical features of regulation by iron and oxygen availability are reflected in regulation of the ProteinHIF - alpha / pVHL interaction. |
| Score | Text |
|---|---|
| 0.9975 | It has recently been shown that HIF - alpha undergoes an iron - and oxygen - dependent modification before it can interact with ProteinpVHL , and that this results in hydroxylation of at least one prolyl residue ( HIF - 1alpha, Pro 564 ). |
| 0.9639 | It has recently been shown that HIF - alpha undergoes an iron - and oxygen - dependent modification before it can interact with pVHL, and that this results in Hydroxylationhydroxylation of at least one prolyl residue ( HIF - 1alpha, Pro 564 ). |
| 0.8824 | It has recently been shown that HIF - alpha undergoes an iron - and oxygen - dependent modification before it can interact with pVHL, and that this results in hydroxylation of at least one Entityprolyl residue ( HIF - 1alpha, Pro 564 ). |
| 0.8342 | It has recently been shown that HIF - alpha undergoes an iron - and oxygen - dependent modification before it can interact with pVHL, and that this results in hydroxylation of at least one prolyl residue Protein( HIF - 1alpha , Pro 564 ). |
| 0.5357 | It has recently been shown that HIF - alpha undergoes an iron - and oxygen - dependent modification before it can interact with pVHL, and that this results in hydroxylation of at least one prolyl residue ( HIF - 1alpha, EntityPro 564 ) . |
| 0.6449 | It has recently been shown that HIF - alpha undergoes an iron - and oxygen - dependent modification before it can interact with pVHL, and that this results in hydroxylation of at least one Entityprolyl residue ( HIF - 1alpha, Pro 564 ). |
| 0.5868 | It has recently been shown that HIF - alpha undergoes an iron - and oxygen - dependent modification before it can interact with pVHL, and that this results in hydroxylation of at least one prolyl residue ( HIF - 1alpha, Pro Entity564 ) . |
| Score | Text |
|---|---|
| 0.5810 | This modification is catalysed by an enzyme termed ProteinHIF - prolyl hydroxylase ( HIF - PH ), and compatible with all previously described prolyl - 4 - hydroxylases HIF - PH also requires 2 - oxoglutarate as a cosubstrate. |
| Score | Text |
|---|---|
| 0.6904 | The key position of this Hydroxylationhydroxylation in the degradation pathway of HIF - alpha, together with its requirement for molecular dioxygen as a co - substrate, provides the potential for HIF - PH to function directly as a cellular oxygen sensor. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9876 | Promoter DNA_methylationmethylation status of the DNA repair genes hMLH1 and MGMT in gastric carcinoma and metaplastic mucosa. |
| 0.9793 | Promoter methylation status of the DNA repair genes ProteinhMLH1 and MGMT in gastric carcinoma and metaplastic mucosa. |
| 0.9762 | EntityPromoter methylation status of the DNA repair genes hMLH1 and MGMT in gastric carcinoma and metaplastic mucosa. |
| 0.9760 | Promoter methylation status of the DNA repair genes hMLH1 and ProteinMGMT in gastric carcinoma and metaplastic mucosa. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9822 | DNA repair genes human Mut L homologue 1 ( hMLH1 ) and O ( 6 ) - methylguanine - DNA methyltransferase ( MGMT ) have been shown to be DNA_methylationhypermethylated in certain carcinomas. |
| 0.9377 | DNA repair genes human Mut L homologue 1 Protein( hMLH1 ) and O ( 6 ) - methylguanine - DNA methyltransferase ( MGMT ) have been shown to be hypermethylated in certain carcinomas. |
| 0.9351 | DNA repair genes human Mut L homologue 1 ( hMLH1 ) and O ( 6 ) - methylguanine - DNA methyltransferase Protein( MGMT ) have been shown to be hypermethylated in certain carcinomas. |
| 0.9225 | DNA repair genes human Mut L homologue 1 ( hMLH1 ) and ProteinO ( 6 ) - methylguanine - DNA methyltransferase ( MGMT ) have been shown to be hypermethylated in certain carcinomas. |
| 0.8682 | DNA repair genes human ProteinMut L homologue 1 ( hMLH1 ) and O ( 6 ) - methylguanine - DNA methyltransferase ( MGMT ) have been shown to be hypermethylated in certain carcinomas. |
| Score | Text |
|---|---|
| 0.9966 | We studied DNA methylation of CpG islands in hMLH1 and ProteinMGMT in 50 gastric carcinomas and 10 intestinal metaplastic mucosa samples. |
| 0.9955 | We studied DNA methylation of CpG islands in ProteinhMLH1 and MGMT in 50 gastric carcinomas and 10 intestinal metaplastic mucosa samples. |
| 0.8821 | We studied DNA_methylationDNA methylation of CpG islands in hMLH1 and MGMT in 50 gastric carcinomas and 10 intestinal metaplastic mucosa samples. |
| 0.6843 | We studied DNA methylation of EntityCpG islands in hMLH1 and MGMT in 50 gastric carcinomas and 10 intestinal metaplastic mucosa samples. |
| 0.9370 | We studied DNA DNA_methylationmethylation of CpG islands in hMLH1 and MGMT in 50 gastric carcinomas and 10 intestinal metaplastic mucosa samples. |
| 0.6879 | We studied DNA_methylationDNA methylation of CpG islands in hMLH1 and MGMT in 50 gastric carcinomas and 10 intestinal metaplastic mucosa samples. |
| Score | Text |
|---|---|
| 0.9992 | We analyzed the methylation status of hMLH1 and ProteinMGMT using methylation - specific polymerase chain reaction and DNA sequencing analysis. |
| 0.9984 | We analyzed the methylation status of ProteinhMLH1 and MGMT using methylation - specific polymerase chain reaction and DNA sequencing analysis. |
| 0.7930 | We analyzed the DNA_methylationmethylation status of hMLH1 and MGMT using methylation - specific polymerase chain reaction and DNA sequencing analysis. |
| Score | Text |
|---|---|
| 0.9992 | We measured protein levels of ProteinhMLH1 using Western blot and immunohistochemical analysis. |
| Score | Text |
|---|---|
| 0.9871 | CpG island hypermethylation of hMLH1 and ProteinMGMT was detected in 11 ( 22 % ) and 8 ( 16 % ) of the 50 gastric tumors, respectively. |
| 0.9736 | CpG island hypermethylation of ProteinhMLH1 and MGMT was detected in 11 ( 22 % ) and 8 ( 16 % ) of the 50 gastric tumors, respectively. |
| 0.9541 | CpG island DNA_methylationhypermethylation of hMLH1 and MGMT was detected in 11 ( 22 % ) and 8 ( 16 % ) of the 50 gastric tumors, respectively. |
| 0.8572 | EntityCpG island hypermethylation of hMLH1 and MGMT was detected in 11 ( 22 % ) and 8 ( 16 % ) of the 50 gastric tumors, respectively. |
| Score | Text |
|---|---|
| 0.9800 | DNA_methylationHypermethylation of the promoter was more common in intestinal - type gastric carcinomas than in poorly diffuse - type gastric carcinomas ( p = 0. 016 and 0. 021, respectively ; Fisher's exact test ). |
| 0.9627 | Hypermethylation of the Entitypromoter was more common in intestinal - type gastric carcinomas than in poorly diffuse - type gastric carcinomas ( p = 0. 016 and 0. 021, respectively ; Fisher's exact test ). |
| Score | Text |
|---|---|
| 0.9840 | However, hMLH1 promoter DNA_methylationhypermethylation did not coincide with MGMT promoter hypermethylation except in 1 patient. |
| 0.9765 | However, hMLH1 promoter hypermethylation did not coincide with ProteinMGMT promoter hypermethylation except in 1 patient. |
| 0.9746 | However, hMLH1 promoter hypermethylation did not coincide with MGMT promoter DNA_methylationhypermethylation except in 1 patient. |
| 0.9677 | However, ProteinhMLH1 promoter hypermethylation did not coincide with MGMT promoter hypermethylation except in 1 patient. |
| 0.9603 | However, hMLH1 Entitypromoter hypermethylation did not coincide with MGMT promoter hypermethylation except in 1 patient. |
| 0.9508 | However, hMLH1 promoter hypermethylation did not coincide with MGMT Entitypromoter hypermethylation except in 1 patient. |
| Score | Text |
|---|---|
| 0.9816 | DNA_methylationHypermethylation of the hMLH1 promoter but not the MGMT promoter occurred in intestinal metaplastic mucosae. |
| 0.9754 | Hypermethylation of the hMLH1 promoter but not the MGMT Entitypromoter occurred in intestinal metaplastic mucosae. |
| 0.9646 | Hypermethylation of the hMLH1 Entitypromoter but not the MGMT promoter occurred in intestinal metaplastic mucosae. |
| 0.9570 | Hypermethylation of the ProteinhMLH1 promoter but not the MGMT promoter occurred in intestinal metaplastic mucosae. |
| 0.9513 | Hypermethylation of the hMLH1 promoter but not the ProteinMGMT promoter occurred in intestinal metaplastic mucosae. |
| Score | Text |
|---|---|
| 0.9961 | Immunohistochemical analysis revealed a corresponding reduction in ProteinhMLH1 protein expression in some of the intestinal metaplastic mucosae. |
| Score | Text |
|---|---|
| 0.5066 | Our results suggest that at least two types of promoter DNA_methylationmethylation participate in the development of gastric carcinoma. |
| Score | Text |
|---|---|
| 0.9868 | Tumor - specific promoter DNA_methylationhypermethylation of hMLH1 may be an early event in carcinogenesis in the stomach. |
| 0.9857 | Tumor - specific promoter hypermethylation of ProteinhMLH1 may be an early event in carcinogenesis in the stomach. |
| 0.9539 | Tumor - specific Entitypromoter hypermethylation of hMLH1 may be an early event in carcinogenesis in the stomach. |
| Score | Text |
|---|---|
| 0.9987 | ProteinHistone deacetylases and cancer : causes and therapies. |
| Score | Text |
|---|---|
| 0.9995 | Together, Proteinhistone acetyltransferases and histone deacetylases ( HDACs ) determine the acetylation status of histones. |
| 0.9993 | Together, histone acetyltransferases and Proteinhistone deacetylases ( HDACs ) determine the acetylation status of histones. |
| 0.9944 | Together, histone acetyltransferases and histone deacetylases ( HDACs ) determine the acetylation status of Proteinhistones . |
| 0.9809 | Together, histone acetyltransferases and histone deacetylases ( HDACs ) determine the Acetylationacetylation status of histones. |
| Score | Text |
|---|---|
| 0.9544 | This Acetylationacetylation affects the regulation of gene expression, and inhibitors of HDACs have been found to cause growth arrest, differentiation and / or apoptosis of many tumours cells by altering the transcription of a small number of genes. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9634 | Co - and posttranslational modification of the Proteinalpha ( 1B ) - adrenergic receptor : effects on receptor expression and function. |
| Score | Text |
|---|---|
| 0.9103 | We have characterized the maturation, co - and posttranslational modifications, and functional properties of the Proteinalpha ( 1B ) - adrenergic receptor ( AR ) expressed in different mammalian cells transfected using conventional approaches or the Semliki Forest virus system. |
| Score | Text |
|---|---|
| 0.9976 | We found that the Proteinalpha ( 1B ) - AR undergoes N - linked glycosylation as demonstrated by its sensitivity to endoglycosidases and by the effect of tunicamycin on receptor maturation. |
| 0.9517 | We found that the alpha ( 1B ) - AR undergoes GlycosylationN - linked glycosylation as demonstrated by its sensitivity to endoglycosidases and by the effect of tunicamycin on receptor maturation. |
| 0.9726 | We found that the alpha ( 1B ) - AR undergoes N - linked Glycosylationglycosylation as demonstrated by its sensitivity to endoglycosidases and by the effect of tunicamycin on receptor maturation. |
| 0.7185 | We found that the alpha ( 1B ) - AR undergoes GlycosylationN - linked glycosylation as demonstrated by its sensitivity to endoglycosidases and by the effect of tunicamycin on receptor maturation. |
| Score | Text |
|---|---|
| 0.9949 | Pulse - chase labeling experiments in BHK - 21 cells demonstrate that the alpha ( 1B ) - AR is synthesized as a 70 kDa core Glycosylationglycosylated precursor that is converted to the 90 kDa mature form of the receptor with a half - time of approximately 2 h. |
| 0.9939 | Pulse - chase labeling experiments in BHK - 21 cells demonstrate that the Proteinalpha ( 1B ) - AR is synthesized as a 70 kDa core glycosylated precursor that is converted to the 90 kDa mature form of the receptor with a half - time of approximately 2 h. |
| Score | Text |
|---|---|
| 0.9754 | N - Linked Glycosylationglycosylation of the alpha ( 1B ) - AR occurs at four asparagines on the N - terminus of the receptor. |
| 0.9583 | N - Linked glycosylation of the Proteinalpha ( 1B ) - AR occurs at four asparagines on the N - terminus of the receptor. |
| 0.6148 | N - Linked glycosylation of the alpha ( 1B ) - AR occurs at Entityfour asparagines on the N - terminus of the receptor. |
| 0.8108 | N - Linked glycosylation of the alpha ( 1B ) - AR occurs at four Entityasparagines on the N - terminus of the receptor. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9890 | Our findings demonstrate that N - linked glycosylation and phosphorylation, but not palmitoylation or O - linked glycosylation, contribute to the structural heterogeneity of the Proteinalpha ( 1B ) - AR as it is observed in SDS - PAGE. |
| 0.9365 | Our findings demonstrate that GlycosylationN - linked glycosylation and phosphorylation, but not palmitoylation or O - linked glycosylation, contribute to the structural heterogeneity of the alpha ( 1B ) - AR as it is observed in SDS - PAGE. |
| 0.8950 | Our findings demonstrate that N - linked glycosylation and phosphorylation, but not palmitoylation or GlycosylationO - linked glycosylation , contribute to the structural heterogeneity of the alpha ( 1B ) - AR as it is observed in SDS - PAGE. |
| 0.8607 | Our findings demonstrate that N - linked glycosylation and Phosphorylationphosphorylation , but not palmitoylation or O - linked glycosylation, contribute to the structural heterogeneity of the alpha ( 1B ) - AR as it is observed in SDS - PAGE. |
| 0.9494 | Our findings demonstrate that N - linked Glycosylationglycosylation and phosphorylation, but not palmitoylation or O - linked glycosylation, contribute to the structural heterogeneity of the alpha ( 1B ) - AR as it is observed in SDS - PAGE. |
| 0.9211 | Our findings demonstrate that N - linked glycosylation and phosphorylation, but not palmitoylation or O - linked Glycosylationglycosylation , contribute to the structural heterogeneity of the alpha ( 1B ) - AR as it is observed in SDS - PAGE. |
| 0.7408 | Our findings demonstrate that GlycosylationN - linked glycosylation and phosphorylation, but not palmitoylation or O - linked glycosylation, contribute to the structural heterogeneity of the alpha ( 1B ) - AR as it is observed in SDS - PAGE. |
| 0.6591 | Our findings demonstrate that N - linked glycosylation and phosphorylation, but not palmitoylation or GlycosylationO - linked glycosylation, contribute to the structural heterogeneity of the alpha ( 1B ) - AR as it is observed in SDS - PAGE. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9950 | Our findings indicate that the Semliki Forest virus system can provide large amounts of functional and fully glycosylated Proteinalpha ( 1B ) - AR protein suitable for biochemical and structural studies. |
| 0.9950 | Our findings indicate that the Semliki Forest virus system can provide large amounts of functional and fully Glycosylationglycosylated alpha ( 1B ) - AR protein suitable for biochemical and structural studies. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9960 | Binding mode analysis of 3 - ( 4 - benzoyl - 1 - methyl - 1H - 2 - pyrrolyl ) - N - hydroxy - 2 - propenamide : a new synthetic Proteinhistone deacetylase inhibitor inducing histone hyperacetylation, growth inhibition, and terminal cell differentiation. |
| 0.9941 | Binding mode analysis of 3 - ( 4 - benzoyl - 1 - methyl - 1H - 2 - pyrrolyl ) - N - hydroxy - 2 - propenamide : a new synthetic histone deacetylase inhibitor inducing Proteinhistone hyperacetylation, growth inhibition, and terminal cell differentiation. |
| 0.9219 | Binding mode analysis of 3 - ( 4 - benzoyl - 1 - methyl - 1H - 2 - pyrrolyl ) - N - hydroxy - 2 - propenamide : a new synthetic histone deacetylase inhibitor inducing histone Acetylationhyperacetylation , growth inhibition, and terminal cell differentiation. |
| Score | Text |
|---|---|
| 0.9816 | The binding mode of 3 - ( 4 - aroyl - 1H - 2 - pyrrolyl ) - N - hydroxy - 2 - propenamides 1a - c, belonging to a recently reported class of synthetic Proteinhistone deacetylase ( HDAC ) inhibitors ( Massa, S. ; et al. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9998 | Chem. 2001, 44, 2069 - 2072 ), into the new modeled ProteinHDAC1 catalytic core is presented, and enzyme / inhibitor interactions are discussed. |
| Score | Text |
|---|---|
| 0.9996 | ProteinHDAC1 X - ray coordinates were obtained by virtual " mutation " of those of histone deacetylase - like protein, a bacterial HDAC homologue. |
| 0.9798 | HDAC1 X - ray coordinates were obtained by virtual " mutation " of those of Proteinhistone deacetylase - like protein, a bacterial HDAC homologue. |
| Score | Text |
|---|---|
| 0.9995 | In in vitro antimaize HD2 as well as antimouse ProteinHDAC1 assay, compounds 1a - c showed inhibitory activities in the low micromolar range. |
| Score | Text |
|---|---|
| 0.9962 | Similarly, 1a - c are endowed with anti - HDAC activity in vivo : on mouse A20 cells, 1a - c induced histone hyperacetylation leading to a highly increased acetylation level of ProteinH4 as compared to control histones. |
| 0.9948 | Similarly, 1a - c are endowed with anti - HDAC activity in vivo : on mouse A20 cells, 1a - c induced Proteinhistone hyperacetylation leading to a highly increased acetylation level of H4 as compared to control histones. |
| 0.9940 | Similarly, 1a - c are endowed with anti - HDAC activity in vivo : on mouse A20 cells, 1a - c induced histone hyperacetylation leading to a highly increased Acetylationacetylation level of H4 as compared to control histones. |
| 0.9826 | Similarly, 1a - c are endowed with anti - HDAC activity in vivo : on mouse A20 cells, 1a - c induced histone Acetylationhyperacetylation leading to a highly increased acetylation level of H4 as compared to control histones. |
| 0.9749 | Similarly, 1a - c are endowed with anti - HDAC activity in vivo : on mouse A20 cells, 1a - c induced histone hyperacetylation leading to a highly increased acetylation level of H4 as compared to control Proteinhistones . |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9874 | Hypoxia - inducible factor ( HIF ) asparagine hydroxylase is identical to factor inhibiting HIF Protein( FIH ) and is related to the cupin structural family. |
| 0.8119 | Hypoxia - inducible factor ( HIF ) asparagine hydroxylase is identical to Proteinfactor inhibiting HIF ( FIH ) and is related to the cupin structural family. |
| ProteinHypoxia - inducible factor ( HIF ) asparagine hydroxylase is identical to factor inhibiting HIF ( FIH ) and is related to the cupin structural family. | |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9982 | Hydroxylation of an asparagine residue in the C - terminal transactivation domain ( CAD ) of HIF - alpha abrogates interaction with Proteinp300 , preventing transcriptional activation. |
| Score | Text |
|---|---|
| 0.9891 | Yeast two - hybrid assays recently identified factor inhibiting HIF Protein( FIH ) as a protein that associates with the CAD region of HIF - alpha. |
| 0.8293 | Yeast two - hybrid assays recently identified Proteinfactor inhibiting HIF ( FIH ) as a protein that associates with the CAD region of HIF - alpha. |
| 0.5683 | Yeast two - hybrid assays recently identified factor Proteininhibiting HIF ( FIH ) as a protein that associates with the CAD region of HIF - alpha. |
| Score | Text |
|---|---|
| 0.9997 | Since FIH contains certain motifs present in iron - and 2 - OG - dependent oxygenases we investigated whether ProteinFIH was the HIF asparaginyl hydroxylase. |
| 0.9996 | Since ProteinFIH contains certain motifs present in iron - and 2 - OG - dependent oxygenases we investigated whether FIH was the HIF asparaginyl hydroxylase. |
| 0.7733 | Since FIH contains certain motifs present in iron - and 2 - OG - dependent oxygenases we investigated whether FIH was the ProteinHIF asparaginyl hydroxylase . |
| Score | Text |
|---|---|
| 0.9997 | Assays using recombinant FIH and HIF - alpha fragments revealed that ProteinFIH is the enzyme that hydroxylates the CAD asparagine residue, that the activity is directly inhibited by cobalt ( II ) and limited by hypoxia, and that the oxygen in the alcohol of the hydroxyasparagine residue is directly derived from dioxygen. |
| 0.9995 | Assays using recombinant ProteinFIH and HIF - alpha fragments revealed that FIH is the enzyme that hydroxylates the CAD asparagine residue, that the activity is directly inhibited by cobalt ( II ) and limited by hypoxia, and that the oxygen in the alcohol of the hydroxyasparagine residue is directly derived from dioxygen. |
| 0.8158 | Assays using recombinant FIH and HIF - alpha fragments revealed that FIH is the enzyme that Hydroxylationhydroxylates the CAD asparagine residue, that the activity is directly inhibited by cobalt ( II ) and limited by hypoxia, and that the oxygen in the alcohol of the hydroxyasparagine residue is directly derived from dioxygen. |
| Score | Text |
|---|---|
| 0.9999 | Sequence analyses involving ProteinFIH link the 2 - OG oxygenases with members of the cupin superfamily, including Zn ( II ) - utilizing phosphomannose isomerase, revealing structural and evolutionary links between these metal - binding proteins that share common motifs. |
| 0.9628 | Sequence analyses involving FIH link the 2 - OG oxygenases with members of the cupin superfamily, including Zn ( II ) - utilizing Proteinphosphomannose isomerase , revealing structural and evolutionary links between these metal - binding proteins that share common motifs. |
| 0.7164 | Sequence analyses involving FIH link the 2 - OG oxygenases with members of the cupin superfamily, including ProteinZn ( II ) - utilizing phosphomannose isomerase , revealing structural and evolutionary links between these metal - binding proteins that share common motifs. |
| Score | Text |
|---|---|
| 0.9993 | ProteinFIH - 1 is an asparaginyl hydroxylase enzyme that regulates the transcriptional activity of hypoxia - inducible factor. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.8306 | HIF transcriptional activity is suppressed under normoxic conditions by Hydroxylationhydroxylation of an asparagine residue within its C - terminal transactivation domain, blocking association with coactivators. |
| Score | Text |
|---|---|
| 0.9996 | Here we show that the protein ProteinFIH - 1 , previously shown to interact with HIF, is an asparaginyl hydroxylase. |
| Score | Text |
|---|---|
| 0.9989 | Like known hydroxylase enzymes, ProteinFIH - 1 is an Fe ( II ) - dependent enzyme that uses molecular O ( 2 ) to modify its substrate. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9787 | [ alpha ] - Secretase ADAM10 as well as Protein[ alpha ] APPs is reduced in platelets and CSF of Alzheimer disease patients. |
| 0.9684 | [ alpha ] - Secretase ProteinADAM10 as well as [ alpha ] APPs is reduced in platelets and CSF of Alzheimer disease patients. |
| Score | Text |
|---|---|
| 0.9161 | BACKGROUND : Members of membrane - bound disintegrin metalloproteinases ( ADAMs ) were shown to be capable of cleaving amyloid precursor protein Protein( APP ) at the alpha - cleavage site in different cell systems. |
| 0.8861 | BACKGROUND : Members of membrane - bound disintegrin metalloproteinases ( ADAMs ) were shown to be capable of cleaving Proteinamyloid precursor protein ( APP ) at the alpha - cleavage site in different cell systems. |
| Score | Text |
|---|---|
| 0.9979 | One of the candidate alpha - secretases identified in this family is ProteinADAM10 . |
| Score | Text |
|---|---|
| 0.9986 | The present study addresses the following major questions : 1 ) Are the levels of an alpha - secretase candidate ( i. e., ProteinADAM10 ) reduced in accessible cells of Alzheimer Disease ( AD ) patients? 2 ) Are ADAM10 levels in the peripheral cells of AD patients related to a concomitant decrease in alpha APPs? MATERIALS AND METHODS : Western Blot analysis of ADAM10 is performed on platelet homogenates from 33 sporadic AD patients and on 26 age - matched control subjects. |
| 0.9234 | The present study addresses the following major questions : 1 ) Are the levels of an alpha - secretase candidate ( i. e., ADAM10 ) reduced in accessible cells of Alzheimer Disease ( AD ) patients? 2 ) Are ADAM10 levels in the peripheral cells of AD patients related to a concomitant decrease in alpha APPs? MATERIALS AND METHODS : Western Blot analysis of ADAM10 is Proteinperformed on platelet homogenates from 33 sporadic AD patients and on 26 age - matched control subjects. |
| 0.5594 | The present study addresses the following major questions : 1 ) Are the levels of an alpha - secretase candidate ( i. e., ADAM10 ) reduced in accessible cells of Alzheimer Disease ( AD ) patients? 2 ) Are ADAM10 levels in the peripheral cells of AD patients related to a concomitant decrease in alpha ProteinAPPs? MATERIALS AND METHODS : Western Blot analysis of ADAM10 is performed on platelet homogenates from 33 sporadic AD patients and on 26 age - matched control subjects. |
| 0.9990 | The present study addresses the following major questions : 1 ) Are the levels of an alpha - secretase candidate ( i. e., ADAM10 ) reduced in accessible cells of Alzheimer Disease ( AD ) patients? 2 ) Are ADAM10 levels in the peripheral cells of AD patients related to a concomitant decrease in alpha APPs? MATERIALS AND METHODS : Western Blot analysis of ProteinADAM10 is performed on platelet homogenates from 33 sporadic AD patients and on 26 age - matched control subjects. |
| 0.9989 | The present study addresses the following major questions : 1 ) Are the levels of an alpha - secretase candidate ( i. e., ADAM10 ) reduced in accessible cells of Alzheimer Disease ( AD ) patients? 2 ) Are ProteinADAM10 levels in the peripheral cells of AD patients related to a concomitant decrease in alpha APPs? MATERIALS AND METHODS : Western Blot analysis of ADAM10 is performed on platelet homogenates from 33 sporadic AD patients and on 26 age - matched control subjects. |
| 0.6958 | The present study addresses the following major questions : 1 ) Are the levels of an alpha - secretase candidate ( i. e., ADAM10 ) reduced in accessible cells of Alzheimer Disease ( AD ) patients? 2 ) Are ADAM10 levels in the peripheral cells of AD patients related to a concomitant decrease in alpha APPs? ProteinMATERIALS AND METHODS : Western Blot analysis of ADAM10 is performed on platelet homogenates from 33 sporadic AD patients and on 26 age - matched control subjects. |
| 0.6089 | The present study addresses the following major questions : 1 ) Are the levels of an alpha - secretase candidate ( i. e., ADAM10 ) reduced in accessible cells of Alzheimer Disease ( AD ) patients? 2 ) Are ADAM10 levels in the peripheral cells of AD patients related to a concomitant decrease in Proteinalpha APPs? MATERIALS AND METHODS : Western Blot analysis of ADAM10 is performed on platelet homogenates from 33 sporadic AD patients and on 26 age - matched control subjects. |
| 0.6018 | The present study addresses the following major questions : 1 ) Are the levels of an alpha - secretase candidate ( i. e., ADAM10 ) reduced in accessible cells of Alzheimer Disease ( AD ) patients? 2 ) Are ADAM10 levels in the peripheral cells of AD patients related to a concomitant decrease in Proteinalpha APPs? MATERIALS AND METHODS : Western Blot analysis of ADAM10 is performed on platelet homogenates from 33 sporadic AD patients and on 26 age - matched control subjects. |
| 0.5532 | The present study addresses the following major questions : 1 ) Are the levels of an alpha - secretase candidate ( i. e., ADAM10 ) reduced in accessible cells of Alzheimer Disease ( AD ) patients? 2 ) Are ProteinADAM10 levels in the peripheral cells of AD patients related to a concomitant decrease in alpha APPs? MATERIALS AND METHODS : Western Blot analysis of ADAM10 is performed on platelet homogenates from 33 sporadic AD patients and on 26 age - matched control subjects. |
| 0.5130 | The present study addresses the following major questions : 1 ) Are the levels of an alpha - secretase candidate ( i. e., ADAM10 ) reduced in accessible cells of Alzheimer Disease ( AD ) patients? 2 ) Are ADAM10 levels in the peripheral cells of AD patients related to a concomitant decrease in Proteinalpha APPs? MATERIALS AND METHODS : Western Blot analysis of ADAM10 is performed on platelet homogenates from 33 sporadic AD patients and on 26 age - matched control subjects. |
| The present study addresses the following major questions : 1 ) Are the levels of an alpha - secretase candidate ( i. e., ADAM10 ) reduced in accessible cells of Alzheimer Disease ( AD ) patients? 2 ) Are ADAM10 Proteinlevels in the peripheral cells of AD patients related to a concomitant decrease in alpha APPs? MATERIALS AND METHODS : Western Blot analysis of ADAM10 is performed on platelet homogenates from 33 sporadic AD patients and on 26 age - matched control subjects. | |
| Score | Text |
|---|---|
| 0.8160 | Moreover, the levels of alpha - secretase metabolite Protein( alpha APPs ) are tested both in platelets and cerebrospinal fluid ( CSF ) of the same pool of subjects by means of Western blot with a specific antibody. |
| 0.8325 | Moreover, the levels of alpha - secretase metabolite ( alpha ProteinAPPs ) are tested both in platelets and cerebrospinal fluid ( CSF ) of the same pool of subjects by means of Western blot with a specific antibody. |
| 0.5920 | Moreover, the levels of alpha - secretase metabolite Protein( alpha APPs ) are tested both in platelets and cerebrospinal fluid ( CSF ) of the same pool of subjects by means of Western blot with a specific antibody. |
| Score | Text |
|---|---|
| 0.9984 | RESULTS : A significant decrease of platelet ProteinADAM10 levels is observed in patients affected by probable AD when compared to control subjects and this is paralleled by a reduced level of alpha APPs released from platelets. |
| 0.9784 | RESULTS : A significant decrease of platelet ADAM10 levels is observed in patients affected by probable AD when compared to control subjects and this is paralleled by a reduced level of Proteinalpha APPs released from platelets. |
| 0.5995 | RESULTS : A significant decrease of platelet ADAM10 levels is observed in patients affected by probable AD when compared to control subjects and this is paralleled by a reduced level of alpha ProteinAPPs released from platelets. |
| Score | Text |
|---|---|
| 0.9375 | Moreover, in the same pool of AD patients, Proteinalpha APPs levels were reduced concomitantly in CSF. |
| Score | Text |
|---|---|
| 0.9991 | CONCLUSIONS : ProteinADAM10 is expressed in platelets. |
| Score | Text |
|---|---|
| 0.9993 | A reduced level of ProteinADAM10 is observed in platelets obtained from AD patients compared to age - matched controls. |
| Score | Text |
|---|---|
| 0.9992 | Further, in the same pool of AD patients, a qualitatively and quantitatively similar decrease in alpha APPs is present both in Proteinthrombin - activated platelets and CSF, thus suggesting that alterations of APP processing might occur both in the neuronal compartment and peripheral cells. |
| 0.9955 | Further, in the same pool of AD patients, a qualitatively and quantitatively similar decrease in alpha APPs is present both in thrombin - activated platelets and CSF, thus suggesting that alterations of ProteinAPP processing might occur both in the neuronal compartment and peripheral cells. |
| 0.9944 | Further, in the same pool of AD patients, a qualitatively and quantitatively similar decrease in Proteinalpha APPs is present both in thrombin - activated platelets and CSF, thus suggesting that alterations of APP processing might occur both in the neuronal compartment and peripheral cells. |
| 0.9610 | Further, in the same pool of AD patients, a qualitatively and quantitatively similar decrease in alpha ProteinAPPs is present both in thrombin - activated platelets and CSF, thus suggesting that alterations of APP processing might occur both in the neuronal compartment and peripheral cells. |
| 0.5273 | Further, in the same pool of AD patients, a qualitatively and quantitatively similar decrease in Proteinalpha APPs is present both in thrombin - activated platelets and CSF, thus suggesting that alterations of APP processing might occur both in the neuronal compartment and peripheral cells. |
| Score | Text |
|---|---|
| 0.9636 | Reduced expression of the insulin - induced protein 1 and Proteinp41 Arp2 / 3 complex genes in human gastric cancers. |
| 0.9342 | Reduced expression of the Proteininsulin - induced protein 1 and p41 Arp2 / 3 complex genes in human gastric cancers. |
| Reduced expression of the insulin - induced protein 1 and p41 ProteinArp2 / 3 complex genes in human gastric cancers. | |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9857 | Quantitative RT - PCR analysis of the 4 genes showed reduced expression of 2 genes in cancers : Insulin - induced protein 1 ( INSIG1 / CL - 6 ) and p41 Arp2 / 3 complex Protein( p41 - Arc ) . |
| 0.9848 | Quantitative RT - PCR analysis of the 4 genes showed reduced expression of 2 genes in cancers : Insulin - induced protein 1 Protein( INSIG1 / CL - 6 ) and p41 Arp2 / 3 complex ( p41 - Arc ). |
| 0.9452 | Quantitative RT - PCR analysis of the 4 genes showed reduced expression of 2 genes in cancers : Insulin - induced protein 1 ( INSIG1 / CL - 6 ) and Proteinp41 Arp2 / 3 complex ( p41 - Arc ). |
| 0.8389 | Quantitative RT - PCR analysis of the 4 genes showed reduced expression of 2 genes in cancers : ProteinInsulin - induced protein 1 ( INSIG1 / CL - 6 ) and p41 Arp2 / 3 complex ( p41 - Arc ). |
| Score | Text |
|---|---|
| 0.9999 | As for ProteinINSIG1 , a DNA fragment was derived from the edge of a CGI in the promoter region. |
| Score | Text |
|---|---|
| 0.9918 | The edge was methylated in 11 of 22 primary gastric cancers, whereas the center was not DNA_methylationmethylated in any cancer. |
| 0.9909 | The edge was DNA_methylationmethylated in 11 of 22 primary gastric cancers, whereas the center was not methylated in any cancer. |
| 0.9346 | The edge was methylated in 11 of 22 primary gastric cancers, whereas the Entitycenter was not methylated in any cancer. |
| 0.9077 | The Entityedge was methylated in 11 of 22 primary gastric cancers, whereas the center was not methylated in any cancer. |
| Score | Text |
|---|---|
| 0.9984 | ProteinINSIG1 expression was markedly reduced in 19 cancers, including the 11 cancers with the methylation. |
| 0.9950 | INSIG1 expression was markedly reduced in 19 cancers, including the 11 cancers with the DNA_methylationmethylation . |
| Score | Text |
|---|---|
| 0.9992 | By 5 - aza - 2'- deoxycytidine treatment of 5 cell lines with the methylation of the edge, partial restoration of ProteinINSIG1 expression was detected only in 2 of them. |
| 0.9880 | By 5 - aza - 2'- deoxycytidine treatment of 5 cell lines with the methylation of the Entityedge , partial restoration of INSIG1 expression was detected only in 2 of them. |
| 0.9879 | By 5 - aza - 2'- deoxycytidine treatment of 5 cell lines with the DNA_methylationmethylation of the edge, partial restoration of INSIG1 expression was detected only in 2 of them. |
| Score | Text |
|---|---|
| 0.9971 | These data indicated that, although the reduced ProteinINSIG1 expression in cancers was associated with the methylation at the edge of the CGI in the promoter region, the methylation was likely to be a secondary change. |
| 0.9885 | These data indicated that, although the reduced INSIG1 expression in cancers was associated with the DNA_methylationmethylation at the edge of the CGI in the promoter region, the methylation was likely to be a secondary change. |
| 0.8987 | These data indicated that, although the reduced INSIG1 expression in cancers was associated with the methylation at the Entityedge of the CGI in the promoter region, the methylation was likely to be a secondary change. |
| 0.9885 | These data indicated that, although the reduced INSIG1 expression in cancers was associated with the methylation at the edge of the CGI in the promoter region, the DNA_methylationmethylation was likely to be a secondary change. |
| 0.9677 | These data indicated that, although the reduced INSIG1 expression in cancers was associated with the methylation at the edge of the EntityCGI in the promoter region, the methylation was likely to be a secondary change. |
| Score | Text |
|---|---|
| 0.9988 | As for Proteinp41 - Arc , a DNA fragment was derived from a CGI overlapping exon 8, and its methylation did not correlate with its expression. |
| 0.9527 | As for p41 - Arc, a DNA fragment was derived from a CGI overlapping exon 8, and its DNA_methylationmethylation did not correlate with its expression. |
| 0.7971 | As for p41 - Arc, a DNA fragment was derived from a EntityCGI overlapping exon 8 , and its methylation did not correlate with its expression. |
| 0.8021 | As for p41 - Arc, a DNA fragment was derived from a CGI overlapping Entityexon 8 , and its methylation did not correlate with its expression. |
| 0.7886 | As for p41 - Arc, a DNA fragment was derived from a CGI Entityoverlapping exon 8 , and its methylation did not correlate with its expression. |
| Score | Text |
|---|---|
| 0.9939 | However, DNA_methylationmethylation of a CGI in the promoter region with a marked reduction of its expression was observed in 1 of the 22 primary cancers. |
| 0.9069 | However, methylation of a EntityCGI in the promoter region with a marked reduction of its expression was observed in 1 of the 22 primary cancers. |
| Score | Text |
|---|---|
| 0.9999 | INSIG1 and Proteinp41 - Arc are known to be involved in cellular differentiation and morphology, respectively, and it was suggested that their reduced expressions might be involved in gastric cancer development or progression. |
| 0.9998 | ProteinINSIG1 and p41 - Arc are known to be involved in cellular differentiation and morphology, respectively, and it was suggested that their reduced expressions might be involved in gastric cancer development or progression. |
| Score | Text |
|---|---|
| 0.9817 | The kyphoscoliotic type of Ehlers - Danlos syndrome ( type VI ) : differential effects on the hydroxylation of lysine in collagens I and ProteinII revealed by analysis of cross - linked telopeptides from urine. |
| 0.9813 | The kyphoscoliotic type of Ehlers - Danlos syndrome ( type VI ) : differential effects on the Hydroxylationhydroxylation of lysine in collagens I and II revealed by analysis of cross - linked telopeptides from urine. |
| 0.9658 | The kyphoscoliotic type of Ehlers - Danlos syndrome ( type VI ) : differential effects on the hydroxylation of Entitylysine in collagens I and II revealed by analysis of cross - linked telopeptides from urine. |
| Score | Text |
|---|---|
| 0.9796 | The kyphoscoliotic type of Ehlers - Danlos syndrome ( EDS type VIA ) ( OMIM 225400 ) is an autosomal recessive connective tissue disorder that results from mutations in the lysyl hydroxylase 1 gene Protein( PLOD1 ) causing underhydroxylation of lysine residues in tissue collagens, particularly of skin. |
| 0.7973 | The kyphoscoliotic type of Ehlers - Danlos syndrome ( EDS type VIA ) ( OMIM 225400 ) is an autosomal recessive connective tissue disorder that results from mutations in the Proteinlysyl hydroxylase 1 gene ( PLOD1 ) causing underhydroxylation of lysine residues in tissue collagens, particularly of skin. |
| 0.5736 | The kyphoscoliotic type of Ehlers - Danlos syndrome ( EDS type VIA ) ( OMIM 225400 ) is an autosomal recessive connective tissue disorder that results from mutations in the lysyl hydroxylase 1 gene ( PLOD1 ) causing underhydroxylation of Entitylysine residues in tissue collagens, particularly of skin. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9998 | Here we isolated cross - linked peptides containing these residues from the urine of a child with EDS VIA homozygous for a mutation that results in a stop codon and effective null expression of ProteinPLOD1 enzyme activity. |
| Score | Text |
|---|---|
| 0.8610 | Peptides that had originated from bone type I collagen and cartilage Proteintype II collagen were identified. |
| Score | Text |
|---|---|
| 0.9621 | A cross - linked N - telopeptide fraction that is derived from bone type I collagen contained only LP, no HP, which means that the helical lysines at residues 930 of alpha 1 ( I ) and Entity933 of alpha 2 ( I ) of the collagen triple - helix had not been hydroxylated. |
| 0.9561 | A cross - linked N - telopeptide fraction that is derived from bone type I collagen contained only LP, no HP, which means that the helical lysines at residues 930 of alpha 1 ( I ) and 933 of alpha 2 ( I ) of the collagen triple - helix had not been Hydroxylationhydroxylated . |
| 0.9348 | A cross - linked N - telopeptide fraction that is derived from bone type I collagen contained only LP, no HP, which means that the helical lysines at residues 930 of alpha 1 ( I ) and 933 of Proteinalpha 2 ( I ) of the collagen triple - helix had not been hydroxylated. |
| 0.9304 | A cross - linked N - telopeptide fraction that is derived from bone type I collagen contained only LP, no HP, which means that the helical lysines at residues 930 of Proteinalpha 1 ( I ) and 933 of alpha 2 ( I ) of the collagen triple - helix had not been hydroxylated. |
| 0.8707 | A cross - linked N - telopeptide fraction that is derived from bone type I collagen contained only LP, no HP, which means that the helical lysines at Entityresidues 930 of alpha 1 ( I ) and 933 of alpha 2 ( I ) of the collagen triple - helix had not been hydroxylated. |
| 0.9294 | A cross - linked N - telopeptide fraction that is derived from bone type I collagen contained only LP, no HP, which means that the helical lysines at residues Entity930 of alpha 1 ( I ) and 933 of alpha 2 ( I ) of the collagen triple - helix had not been hydroxylated. |
| 0.8101 | A cross - linked N - telopeptide fraction that is derived from bone type I collagen contained only LP, no HP, which means that the helical Entitylysines at residues 930 of alpha 1 ( I ) and 933 of alpha 2 ( I ) of the collagen triple - helix had not been hydroxylated. |
| 0.6139 | A cross - linked N - telopeptide fraction that is derived from bone type I collagen contained only LP, no HP, which means that the helical lysines at residues 930 of alpha 1 ( I ) and 933 of alpha Protein2 ( I ) of the collagen triple - helix had not been hydroxylated. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9532 | A second cross - linked peptide that is derived from the C - telopeptide domain of cartilage Proteintype II collagen showed both HP and LP in a 2 : 1 ratio, compared with 18 : 1 for the equivalent peptide from a normal child's urine. |
| Score | Text |
|---|---|
| 0.9299 | The results show that in EDS VIA, bone type I collagen is more markedly underhydroxylated than cartilage Proteintype II collagen , at least at those helical sites that form cross - links. |
| 0.2504 | The results show that in EDS VIA, bone type I collagen is more markedly Glycosylationunderhydroxylated than cartilage type II collagen, at least at those helical sites that form cross - links. |
| The results show that in EDS VIA, bone type I collagen is more markedly Hydroxylationunderhydroxylated than cartilage type II collagen, at least at those helical sites that form cross - links. | |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9989 | Since ProteinPLOD1 is null, other PLOD genes must be responsible for the helical hydroxylation activity that results in HP. |
| Score | Text |
|---|---|
| 0.9348 | The presented approach of analyzing urinary cross - linked C - telopeptide fragments of Proteintype II collagen may allow the detection of chondrodysplasias due to genetic defects in lysyl hydroxylase isoforms active in cartilage. |
| Score | Text |
|---|---|
| 0.9843 | Postsynthetic Methylationtrimethylation of histone H4 at lysine 20 in mammalian tissues is associated with aging. |
| 0.8944 | Postsynthetic trimethylation of Proteinhistone H4 at lysine 20 in mammalian tissues is associated with aging. |
| 0.8836 | Postsynthetic trimethylation of histone H4 at Entitylysine 20 in mammalian tissues is associated with aging. |
| Score | Text |
|---|---|
| 0.9641 | Methylation of the N - terminal region of Proteinhistones was first described more than 35 years ago, but its biological significance has remained unclear. |
| 0.8936 | Methylation of the EntityN - terminal region of histones was first described more than 35 years ago, but its biological significance has remained unclear. |
| 0.8667 | MethylationMethylation of the N - terminal region of histones was first described more than 35 years ago, but its biological significance has remained unclear. |
| 0.8506 | Methylation of the EntityN - terminal region of histones was first described more than 35 years ago, but its biological significance has remained unclear. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9948 | Primarily because of the recent discovery of the SET domain - depending H3 - specific histone methyltransferases SUV39H1 and ProteinSuv39h1 , which selectively methylate lysine 9 of the H3 N terminus, this posttranslational modification has regained scientific interest. |
| 0.9940 | Primarily because of the recent discovery of the SET domain - depending H3 - specific histone methyltransferases ProteinSUV39H1 and Suv39h1, which selectively methylate lysine 9 of the H3 N terminus, this posttranslational modification has regained scientific interest. |
| 0.9753 | Primarily because of the recent discovery of the SET domain - depending H3 - specific histone methyltransferases SUV39H1 and Suv39h1, which selectively methylate lysine 9 of the ProteinH3 N terminus, this posttranslational modification has regained scientific interest. |
| 0.9666 | Primarily because of the recent discovery of the SET domain - depending ProteinH3 - specific histone methyltransferases SUV39H1 and Suv39h1, which selectively methylate lysine 9 of the H3 N terminus, this posttranslational modification has regained scientific interest. |
| 0.9609 | Primarily because of the recent discovery of the SET domain - depending H3 - specific histone methyltransferases SUV39H1 and Suv39h1, which selectively methylate Entitylysine 9 of the H3 N terminus, this posttranslational modification has regained scientific interest. |
| 0.9606 | Primarily because of the recent discovery of the SET domain - depending H3 - specific Proteinhistone methyltransferases SUV39H1 and Suv39h1, which selectively methylate lysine 9 of the H3 N terminus, this posttranslational modification has regained scientific interest. |
| 0.5045 | Primarily because of the recent discovery of the SET domain - depending H3 - specific histone methyltransferases SUV39H1 and Suv39h1, which selectively Methylationmethylate lysine 9 of the H3 N terminus, this posttranslational modification has regained scientific interest. |
| 0.9751 | Primarily because of the recent discovery of the SET domain - depending ProteinH3 - specific histone methyltransferases SUV39H1 and Suv39h1, which selectively methylate lysine 9 of the H3 N terminus, this posttranslational modification has regained scientific interest. |
| 0.7632 | Primarily because of the recent discovery of the SET domain - depending H3 - specific histone methyltransferases SUV39H1 and Suv39h1, which selectively methylate Entitylysine 9 of the H3 N terminus, this posttranslational modification has regained scientific interest. |
| Primarily because of the recent discovery of the SET domain - depending H3 - specific histone methyltransferases SUV39H1 and Suv39h1, which selectively Catalysismethylate lysine 9 of the H3 N terminus, this posttranslational modification has regained scientific interest. | |
| Score | Text |
|---|---|
| 0.9890 | In the past, investigations concerning the biological significance of histone Methylationmethylation were largely limited because of a lack of simple and sensitive analytical procedures for detecting this modification. |
| 0.9868 | In the past, investigations concerning the biological significance of Proteinhistone methylation were largely limited because of a lack of simple and sensitive analytical procedures for detecting this modification. |
| Score | Text |
|---|---|
| 0.9893 | The present work investigated the Methylationmethylation pattern of histone H4 both in different mammalian organs of various ages and in cell lines by applying mass spectrometric analysis and a newly developed hydrophilic - interaction liquid chromatographic method enabling the simultaneous separation of methylated and acetylated forms, which obviates the need to work with radioactive materials. |
| 0.9753 | The present work investigated the methylation pattern of Proteinhistone H4 both in different mammalian organs of various ages and in cell lines by applying mass spectrometric analysis and a newly developed hydrophilic - interaction liquid chromatographic method enabling the simultaneous separation of methylated and acetylated forms, which obviates the need to work with radioactive materials. |
| 0.7084 | The present work investigated the methylation pattern of histone H4 both in different mammalian organs of various ages and in cell lines by applying mass spectrometric analysis and a newly developed hydrophilic - interaction liquid chromatographic method enabling the simultaneous separation of Methylationmethylated and acetylated forms, which obviates the need to work with radioactive materials. |
| 0.7025 | The present work investigated the methylation pattern of histone H4 both in different mammalian organs of various ages and in cell lines by applying mass spectrometric analysis and a newly developed hydrophilic - interaction liquid chromatographic method enabling the simultaneous separation of methylated and Acetylationacetylated forms, which obviates the need to work with radioactive materials. |
| Score | Text |
|---|---|
| 0.9705 | In rat kidney and liver the Methylationdimethylated lysine 20 was found to be the main methylation product, whereas the monomethyl derivative was present in much smaller amounts. |
| 0.9286 | In rat kidney and liver the dimethylated lysine 20 was found to be the main methylation product, whereas the Methylationmonomethyl derivative was present in much smaller amounts. |
| 0.9131 | In rat kidney and liver the dimethylated Entitylysine 20 was found to be the main methylation product, whereas the monomethyl derivative was present in much smaller amounts. |
| 0.6436 | In rat kidney and liver the dimethylated Entitylysine 20 was found to be the main methylation product, whereas the monomethyl derivative was present in much smaller amounts. |
| 0.5199 | In rat kidney and liver the dimethylated lysine 20 was found to be the main Methylationmethylation product, whereas the monomethyl derivative was present in much smaller amounts. |
| Score | Text |
|---|---|
| 0.9797 | In addition, for the first time a Methylationtrimethylated form of lysine 20 of H4 was found in mammalian tissue. |
| 0.9664 | In addition, for the first time a trimethylated form of lysine 20 of ProteinH4 was found in mammalian tissue. |
| 0.9549 | In addition, for the first time a trimethylated form of Entitylysine 20 of H4 was found in mammalian tissue. |
| 0.6508 | In addition, for the first time a trimethylated form of Entitylysine 20 of H4 was found in mammalian tissue. |
| Score | Text |
|---|---|
| 0.9849 | A significant increase in this Methylationtrimethylated histone H4 was detected in organs of animals older than 30 days, whereas the amounts of mono - and dimethylated forms did not essentially change in organs from young ( 10 days old ) or old animals ( 30 and 450 days old ). |
| 0.9770 | A significant increase in this trimethylated histone H4 was detected in organs of animals older than 30 days, whereas the amounts of mono - and Methylationdimethylated forms did not essentially change in organs from young ( 10 days old ) or old animals ( 30 and 450 days old ). |
| 0.9747 | A significant increase in this trimethylated histone H4 was detected in organs of animals older than 30 days, whereas the amounts of Methylationmono - and dimethylated forms did not essentially change in organs from young ( 10 days old ) or old animals ( 30 and 450 days old ). |
| 0.9511 | A significant increase in this trimethylated Proteinhistone H4 was detected in organs of animals older than 30 days, whereas the amounts of mono - and dimethylated forms did not essentially change in organs from young ( 10 days old ) or old animals ( 30 and 450 days old ). |
| Score | Text |
|---|---|
| 0.9964 | Trimethylated ProteinH4 was also detected in transformed cells ; although it was present in only trace amounts in logarithmically growing cells, we found an increase in trimethylated lysine 20 in cells in the stationary phase. |
| 0.9951 | Trimethylated H4 was also detected in transformed cells ; although it was present in only trace amounts in logarithmically growing cells, we found an increase in Methylationtrimethylated lysine 20 in cells in the stationary phase. |
| 0.9903 | MethylationTrimethylated H4 was also detected in transformed cells ; although it was present in only trace amounts in logarithmically growing cells, we found an increase in trimethylated lysine 20 in cells in the stationary phase. |
| 0.9192 | Trimethylated H4 was also detected in transformed cells ; although it was present in only trace amounts in logarithmically growing cells, we found an increase in trimethylated Entitylysine 20 in cells in the stationary phase. |
| Score | Text |
|---|---|
| 0.9734 | In the Proteincystathionine beta - synthase knockout mouse, elevations in total plasma homocysteine increase tissue S - adenosylhomocysteine, but responses of S - adenosylmethionine and DNA methylation are tissue specific. |
| Score | Text |
|---|---|
| 0.9700 | The Proteincystathionine beta - synthase knockout mouse provides a unique opportunity to study biochemical consequences of a defective cystathionine beta - synthase enzyme. |
| 0.9385 | The cystathionine beta - synthase knockout mouse provides a unique opportunity to study biochemical consequences of a defective Proteincystathionine beta - synthase enzyme. |
| Score | Text |
|---|---|
| 0.9727 | The present study was undertaken to assess the effect of elevated plasma total homocysteine caused by Proteincystathionine beta - synthase deficiency on one - carbon metabolism in 10 homozygous mutant mice and 10 age - and sex - matched wild - type mice. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9716 | The results of this study are consistent with the predicted role of Proteincystathionine beta - synthase in the regulation of plasma total homocysteine levels and tissue S - adenosylhomocysteine levels. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9720 | GlycosylationGlycosylation of human proteinase - activated receptor - 2 ( hPAR2 ) : role in cell surface expression and signalling. |
| 0.9486 | Glycosylation of human proteinase - activated receptor - 2 Protein( hPAR2 ) : role in cell surface expression and signalling. |
| 0.6816 | Glycosylation of human Proteinproteinase - activated receptor - 2 ( hPAR2 ) : role in cell surface expression and signalling. |
| Score | Text |
|---|---|
| 0.9764 | We have analysed the role of N - linked glycosylation in regulating human proteinase - activated receptor - 2 Protein( hPAR ( 2 ) ) expression and function. |
| 0.9109 | We have analysed the role of GlycosylationN - linked glycosylation in regulating human proteinase - activated receptor - 2 ( hPAR ( 2 ) ) expression and function. |
| 0.7643 | We have analysed the role of N - linked glycosylation in regulating human Proteinproteinase - activated receptor - 2 ( hPAR ( 2 ) ) expression and function. |
| 0.9603 | We have analysed the role of N - linked Glycosylationglycosylation in regulating human proteinase - activated receptor - 2 ( hPAR ( 2 ) ) expression and function. |
| 0.5297 | We have analysed the role of GlycosylationN - linked glycosylation in regulating human proteinase - activated receptor - 2 ( hPAR ( 2 ) ) expression and function. |
| Score | Text |
|---|---|
| 0.9991 | Epitope - tagged wild - type hPAR ( 2 ) ( wt - hPAR ( 2 ) ) or ProteinhPAR ( 2 ) that lacked glycosylation sequons ( following site - directed mutagenesis ) in either the N - terminus [ hPAR ( 2 ) N30A ( Asn ( 30 ) - - > Ala ) ], extracellular loop 2 [ ECL2 ; hPAR ( 2 ) N222Q ( Asn ( 222 ) - - > Gln ) or hPAR ( 2 ) N222A ( Asn ( 222 ) - - > Ala ) ] or both ( hPAR ( 2 ) N30A, N222A or hPAR ( 2 ) N30A, N222Q ) were expressed in the Chinese - hamster ovary ( CHO ) fibroblast cell line, Pro5. |
| 0.9989 | Epitope - tagged wild - type ProteinhPAR ( 2 ) ( wt - hPAR ( 2 ) ) or hPAR ( 2 ) that lacked glycosylation sequons ( following site - directed mutagenesis ) in either the N - terminus [ hPAR ( 2 ) N30A ( Asn ( 30 ) - - > Ala ) ], extracellular loop 2 [ ECL2 ; hPAR ( 2 ) N222Q ( Asn ( 222 ) - - > Gln ) or hPAR ( 2 ) N222A ( Asn ( 222 ) - - > Ala ) ] or both ( hPAR ( 2 ) N30A, N222A or hPAR ( 2 ) N30A, N222Q ) were expressed in the Chinese - hamster ovary ( CHO ) fibroblast cell line, Pro5. |
| 0.9968 | Epitope - tagged wild - type hPAR ( 2 ) Protein( wt - hPAR ( 2 ) ) or hPAR ( 2 ) that lacked glycosylation sequons ( following site - directed mutagenesis ) in either the N - terminus [ hPAR ( 2 ) N30A ( Asn ( 30 ) - - > Ala ) ], extracellular loop 2 [ ECL2 ; hPAR ( 2 ) N222Q ( Asn ( 222 ) - - > Gln ) or hPAR ( 2 ) N222A ( Asn ( 222 ) - - > Ala ) ] or both ( hPAR ( 2 ) N30A, N222A or hPAR ( 2 ) N30A, N222Q ) were expressed in the Chinese - hamster ovary ( CHO ) fibroblast cell line, Pro5. |
| 0.9940 | Epitope - tagged wild - type hPAR ( 2 ) ( wt - hPAR ( 2 ) ) or hPAR ( 2 ) that lacked glycosylation sequons ( following site - directed mutagenesis ) in either the N - terminus [ hPAR ( 2 ) N30A ( Asn ( 30 ) - - > Ala ) ], extracellular loop 2 [ ECL2 ; hPAR ( 2 ) N222Q ( Asn ( 222 ) - - > Gln ) or hPAR ( 2 ) N222A ( Asn ( 222 ) - - > Ala ) ] or both ( hPAR ( 2 ) N30A, N222A or ProteinhPAR ( 2 ) N30A , N222Q ) were expressed in the Chinese - hamster ovary ( CHO ) fibroblast cell line, Pro5. |
| 0.9907 | Epitope - tagged wild - type hPAR ( 2 ) ( wt - hPAR ( 2 ) ) or hPAR ( 2 ) that lacked glycosylation sequons ( following site - directed mutagenesis ) in either the N - terminus [ hPAR ( 2 ) N30A ( Asn ( 30 ) - - > Ala ) ], extracellular loop 2 [ ECL2 ; hPAR ( 2 ) N222Q ( Asn ( 222 ) - - > Gln ) or hPAR ( 2 ) N222A ( Asn ( 222 ) - - > Ala ) ] or both Protein( hPAR ( 2 ) N30A , N222A or hPAR ( 2 ) N30A, N222Q ) were expressed in the Chinese - hamster ovary ( CHO ) fibroblast cell line, Pro5. |
| 0.9727 | Epitope - tagged wild - type hPAR ( 2 ) ( wt - hPAR ( 2 ) ) or hPAR ( 2 ) that lacked glycosylation sequons ( following site - directed mutagenesis ) in either the N - terminus Protein[ hPAR ( 2 ) N30A ( Asn ( 30 ) - - > Ala ) ], extracellular loop 2 [ ECL2 ; hPAR ( 2 ) N222Q ( Asn ( 222 ) - - > Gln ) or hPAR ( 2 ) N222A ( Asn ( 222 ) - - > Ala ) ] or both ( hPAR ( 2 ) N30A, N222A or hPAR ( 2 ) N30A, N222Q ) were expressed in the Chinese - hamster ovary ( CHO ) fibroblast cell line, Pro5. |
| 0.9585 | Epitope - tagged wild - type hPAR ( 2 ) ( wt - hPAR ( 2 ) ) or hPAR ( 2 ) that lacked glycosylation sequons ( following site - directed mutagenesis ) in either the N - terminus [ hPAR ( 2 ) N30A ( Asn ( 30 ) - - > Ala ) ], extracellular loop 2 [ ECL2 ; hPAR ( 2 ) N222Q ( Asn ( 222 ) - - > Gln ) or ProteinhPAR ( 2 ) N222A ( Asn ( 222 ) - - > Ala ) ] or both ( hPAR ( 2 ) N30A, N222A or hPAR ( 2 ) N30A, N222Q ) were expressed in the Chinese - hamster ovary ( CHO ) fibroblast cell line, Pro5. |
| 0.8938 | Epitope - tagged wild - type hPAR ( 2 ) ( wt - hPAR ( 2 ) ) or hPAR ( 2 ) that lacked glycosylation sequons ( following site - directed mutagenesis ) in either the N - terminus [ hPAR ( 2 ) N30A ( Asn ( 30 ) - - > Ala ) ], extracellular loop 2 [ ECL2 ; ProteinhPAR ( 2 ) N222Q ( Asn ( 222 ) - - > Gln ) or hPAR ( 2 ) N222A ( Asn ( 222 ) - - > Ala ) ] or both ( hPAR ( 2 ) N30A, N222A or hPAR ( 2 ) N30A, N222Q ) were expressed in the Chinese - hamster ovary ( CHO ) fibroblast cell line, Pro5. |
| 0.9945 | Epitope - tagged wild - type ProteinhPAR ( 2 ) ( wt - hPAR ( 2 ) ) or hPAR ( 2 ) that lacked glycosylation sequons ( following site - directed mutagenesis ) in either the N - terminus [ hPAR ( 2 ) N30A ( Asn ( 30 ) - - > Ala ) ], extracellular loop 2 [ ECL2 ; hPAR ( 2 ) N222Q ( Asn ( 222 ) - - > Gln ) or hPAR ( 2 ) N222A ( Asn ( 222 ) - - > Ala ) ] or both ( hPAR ( 2 ) N30A, N222A or hPAR ( 2 ) N30A, N222Q ) were expressed in the Chinese - hamster ovary ( CHO ) fibroblast cell line, Pro5. |
| Score | Text |
|---|---|
| 0.9982 | Western blot analysis of Proteinwt - hPAR ( 2 ) showed mature wt - hPAR ( 2 ) to have a molecular mass of 55 - 100 kDa, and 33 - 48 kDa following N - glycosidase F deglycosylation. |
| 0.9982 | Western blot analysis of wt - hPAR ( 2 ) showed mature Proteinwt - hPAR ( 2 ) to have a molecular mass of 55 - 100 kDa, and 33 - 48 kDa following N - glycosidase F deglycosylation. |
| 0.9305 | Western blot analysis of wt - hPAR ( 2 ) showed mature wt - hPAR ( 2 ) to have a molecular mass of 55 - 100 kDa, and 33 - 48 kDa following ProteinN - glycosidase F deglycosylation. |
| 0.4976 | Western blot analysis of wt - hPAR ( 2 ) showed mature wt - hPAR ( 2 ) to have a molecular mass of 55 - 100 kDa, and 33 - 48 kDa following N - glycosidase F Catalysisdeglycosylation . |
| 0.9227 | Western blot analysis of wt - hPAR ( 2 ) showed mature wt - hPAR ( 2 ) to have a molecular mass of 55 - 100 kDa, and 33 - 48 kDa following N Protein- glycosidase F deglycosylation. |
| Western blot analysis of wt - hPAR ( 2 ) showed mature wt - hPAR ( 2 ) to have a molecular mass of 55 - 100 kDa, and 33 - 48 kDa following N - glycosidase F Deglycosylationdeglycosylation . | |
| Score | Text |
|---|---|
| 0.9998 | FACS analysis and immunocytochemistry of the Proteinwt - hPAR ( 2 ) and PAR ( 2 ) mutant cell lines revealed that removal of both glycosylation sequons decreases ( 50 % of wt - hPAR ( 2 ) ) cell surface expression. |
| 0.9998 | FACS analysis and immunocytochemistry of the wt - hPAR ( 2 ) and PAR ( 2 ) mutant cell lines revealed that removal of both glycosylation sequons decreases ( 50 % of Proteinwt - hPAR ( 2 ) ) cell surface expression. |
| 0.9998 | FACS analysis and immunocytochemistry of the wt - hPAR ( 2 ) and ProteinPAR ( 2 ) mutant cell lines revealed that removal of both glycosylation sequons decreases ( 50 % of wt - hPAR ( 2 ) ) cell surface expression. |
| Score | Text |
|---|---|
| 0.9885 | Western blot analysis indicated that both N - linked sites are Glycosylationglycosylated . |
| 0.7699 | Western blot analysis indicated that both EntityN - linked sites are glycosylated. |
| 0.6745 | Western blot analysis indicated that both EntityN - linked sites are glycosylated. |
| Score | Text |
|---|---|
| 0.9994 | In functional studies, ProteinhPAR ( 2 ) N30A displayed a selective and significant increase in sensitivity towards tryptase. |
| Score | Text |
|---|---|
| 0.9993 | Interestingly, hPAR ( 2 ) N222A displayed a loss in sensitivity towards all ProteinPAR ( 2 ) agonists tested. |
| 0.9946 | Interestingly, ProteinhPAR ( 2 ) N222A displayed a loss in sensitivity towards all PAR ( 2 ) agonists tested. |
| Score | Text |
|---|---|
| 0.9997 | However, further analysis revealed receptor sensitivity to alanine mutations in this domain, as the more conservative substitution hPAR ( 2 ) N222Q displayed no change in response to ProteinPAR ( 2 ) agonists. hPAR ( 2 ) N30A, N222Q displayed increased sensitivity towards tryptase, but a loss in sensitivity towards trypsin and the synthetic peptide SLIGRL - NH ( 2 ), although this loss in sensitivity towards trypsin and SLIGRL - NH ( 2 ) was secondary to changes in cell - surface expression. |
| 0.9980 | However, further analysis revealed receptor sensitivity to alanine mutations in this domain, as the more conservative substitution hPAR ( 2 ) N222Q displayed no change in response to PAR ( 2 ) agonists. ProteinhPAR ( 2 ) N30A , N222Q displayed increased sensitivity towards tryptase, but a loss in sensitivity towards trypsin and the synthetic peptide SLIGRL - NH ( 2 ), although this loss in sensitivity towards trypsin and SLIGRL - NH ( 2 ) was secondary to changes in cell - surface expression. |
| 0.9931 | However, further analysis revealed receptor sensitivity to alanine mutations in this domain, as the more conservative substitution ProteinhPAR ( 2 ) N222Q displayed no change in response to PAR ( 2 ) agonists. hPAR ( 2 ) N30A, N222Q displayed increased sensitivity towards tryptase, but a loss in sensitivity towards trypsin and the synthetic peptide SLIGRL - NH ( 2 ), although this loss in sensitivity towards trypsin and SLIGRL - NH ( 2 ) was secondary to changes in cell - surface expression. |
| 0.9966 | However, further analysis revealed receptor sensitivity to alanine mutations in this domain, as the more conservative substitution hPAR ( 2 ) N222Q displayed no change in response to PAR ( 2 ) agonists. hPAR ( 2 ) N30A, N222Q displayed increased sensitivity towards tryptase, but a loss in sensitivity towards trypsin and the synthetic peptide ProteinSLIGRL - NH ( 2 ) , although this loss in sensitivity towards trypsin and SLIGRL - NH ( 2 ) was secondary to changes in cell - surface expression. |
| 0.9243 | However, further analysis revealed receptor sensitivity to alanine mutations in this domain, as the more conservative substitution hPAR ( 2 ) N222Q displayed no change in response to PAR ( 2 ) agonists. hPAR ( 2 ) N30A, N222Q displayed increased sensitivity towards tryptase, but a loss in sensitivity towards trypsin and the synthetic peptide SLIGRL - NH ( 2 ), although this loss in sensitivity towards trypsin and ProteinSLIGRL - NH ( 2 ) was secondary to changes in cell - surface expression. |
| Score | Text |
|---|---|
| 0.9994 | Finally, expression of sialic - acid - deficient Proteinwt - hPAR ( 2 ) in the CHO Lec2 glycosylation - deficient mutant cell line, showed a 40 kDa loss in molecular mass, in addition to a marked and selective increase in sensitivity towards tryptase. |
| Score | Text |
|---|---|
| 0.9991 | We conclude that ProteinhPAR ( 2 ) N - linked glycosylation and sialylation regulates receptor expression and / or signalling. |
| 0.8338 | We conclude that hPAR ( 2 ) GlycosylationN - linked glycosylation and sialylation regulates receptor expression and / or signalling. |
| 0.8733 | We conclude that hPAR ( 2 ) N - linked Glycosylationglycosylation and sialylation regulates receptor expression and / or signalling. |
| 0.6257 | We conclude that hPAR ( 2 ) GlycosylationN - linked glycosylation and sialylation regulates receptor expression and / or signalling. |
| Score | Text |
|---|---|
| 0.9201 | ProteinN - acetyltransferase 2 genotype - related sulfapyridine acetylation and its adverse events. |
| Score | Text |
|---|---|
| 0.9802 | Sulfapyridine ( SP ), one of the metabolites of sulfasalazine ( SASP ), is further metabolized into N - acetylsulfapyridine ( AcSP ) by polymorphic N - acetyltransferase 2 Protein( NAT2 ) . |
| 0.8200 | Sulfapyridine ( SP ), one of the metabolites of sulfasalazine ( SASP ), is further metabolized into N - acetylsulfapyridine ( AcSP ) by polymorphic ProteinN - acetyltransferase 2 ( NAT2 ). |
| Score | Text |
|---|---|
| 0.9994 | ProteinNAT2 activity has been diagnosed by phenotyping, that is, evaluating plasma concentrations or urinary excretions of tentatively administered test drugs for dose individualization and avoidance of serious adverse events. |
| Score | Text |
|---|---|
| 0.9999 | Herein, we investigated the relationship between ProteinNAT2 genotypes and the pharmacokinetics of SP in healthy Japanese subjects, as well as the adverse events of SASP in patients with inflammatory bowel disease ( IBD ). |
| Score | Text |
|---|---|
| 0.9997 | Eight healthy subjects and 13 IBD patients were classified into three groups by ProteinNAT2 genotyping ; the homozygote for the wild - type allele ( Rapid Types ), the compound heterozygote for the wild - type and mutant alleles ( Intermediate Types ), and the homozygote for mutant alleles ( Slow Types ). |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9997 | The ProteinNAT2 genotypes were well - correlated with the plasma concentrations or urinary excretions of SP and AcSP in 8 healthy subjects, except for one Slow Type. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9997 | In this case, the ProteinNAT2 activity was diagnosed by genotyping in advance, and the medical staff could pay scrupulous attention, resulting in no serious subjective symptoms such as abdominal pain, anorexia or fever. |
| Score | Text |
|---|---|
| 0.9999 | Further investigations on the relationship between the ProteinNAT2 genotype and adverse events are required, although genotyping appeared to be a promising method to avoid such serious adverse events. |
| Score | Text |
|---|---|
| 0.9994 | Histone H3 lysine 4 methylation is mediated by ProteinSet1 and promotes maintenance of active chromatin states in fission yeast. |
| 0.9720 | Histone H3 lysine 4 Methylationmethylation is mediated by Set1 and promotes maintenance of active chromatin states in fission yeast. |
| 0.8466 | ProteinHistone H3 lysine 4 methylation is mediated by Set1 and promotes maintenance of active chromatin states in fission yeast. |
| 0.7979 | Histone H3 Entitylysine 4 methylation is mediated by Set1 and promotes maintenance of active chromatin states in fission yeast. |
| 0.6807 | Histone H3 lysine 4 methylation is Catalysismediated by Set1 and promotes maintenance of active chromatin states in fission yeast. |
| Score | Text |
|---|---|
| 0.9432 | Methylation of Proteinhistone H3 at lysine 4 ( H3 Lys - 4 ) or lysine 9 ( H3 Lys - 9 ) is known to define active and silent chromosomal domains respectively from fission yeast to humans. |
| 0.9095 | MethylationMethylation of histone H3 at lysine 4 ( H3 Lys - 4 ) or lysine 9 ( H3 Lys - 9 ) is known to define active and silent chromosomal domains respectively from fission yeast to humans. |
| 0.8615 | Methylation of histone H3 at lysine 4 ( H3 Lys - 4 ) or lysine 9 ( H3 EntityLys - 9 ) is known to define active and silent chromosomal domains respectively from fission yeast to humans. |
| 0.8457 | Methylation of histone H3 at Entitylysine 4 ( H3 Lys - 4 ) or lysine 9 ( H3 Lys - 9 ) is known to define active and silent chromosomal domains respectively from fission yeast to humans. |
| 0.8383 | Methylation of histone H3 at lysine 4 ( H3 Lys - 4 ) or Entitylysine 9 ( H3 Lys - 9 ) is known to define active and silent chromosomal domains respectively from fission yeast to humans. |
| 0.7948 | Methylation of histone H3 at lysine 4 ( H3 EntityLys - 4 ) or lysine 9 ( H3 Lys - 9 ) is known to define active and silent chromosomal domains respectively from fission yeast to humans. |
| 0.6926 | Methylation of histone H3 at lysine 4 ( H3 Lys - 4 ) or lysine 9 Protein( H3 Lys - 9 ) is known to define active and silent chromosomal domains respectively from fission yeast to humans. |
| 0.6748 | Methylation of histone H3 at lysine 4 Protein( H3 Lys - 4 ) or lysine 9 ( H3 Lys - 9 ) is known to define active and silent chromosomal domains respectively from fission yeast to humans. |
| 0.5307 | Methylation of histone H3 at lysine 4 ( H3 Lys - 4 ) or lysine 9 Entity( H3 Lys - 9 ) is known to define active and silent chromosomal domains respectively from fission yeast to humans. |
| 0.4543 | Methylation of histone H3 at lysine 4 Entity( H3 Lys - 4 ) or lysine 9 ( H3 Lys - 9 ) is known to define active and silent chromosomal domains respectively from fission yeast to humans. |
| Score | Text |
|---|---|
| 0.9806 | However, in budding yeast, H3 Lys - 4 Methylationmethylation is also necessary for silent chromatin assembly at telomeres and ribosomal DNA. |
| 0.9711 | However, in budding yeast, H3 EntityLys - 4 methylation is also necessary for silent chromatin assembly at telomeres and ribosomal DNA. |
| 0.9638 | However, in budding yeast, ProteinH3 Lys - 4 methylation is also necessary for silent chromatin assembly at telomeres and ribosomal DNA. |
| Score | Text |
|---|---|
| 0.9995 | Here we demonstrate that deletion of Proteinset1 , which encodes a protein containing an RNA recognition motif at its amino terminus and a SET domain at the carboxy terminus, abolishes H3 Lys - 4 methylation in fission yeast. |
| 0.9882 | Here we demonstrate that deletion of set1, which encodes a protein containing an RNA recognition motif at its amino terminus and a SET domain at the carboxy terminus, abolishes ProteinH3 Lys - 4 methylation in fission yeast. |
| 0.9817 | Here we demonstrate that deletion of set1, which encodes a protein containing an RNA recognition motif at its amino terminus and a SET domain at the carboxy terminus, abolishes H3 EntityLys - 4 methylation in fission yeast. |
| 0.9727 | Here we demonstrate that deletion of set1, which encodes a protein containing an RNA recognition motif at its amino terminus and a SET domain at the carboxy terminus, abolishes H3 Lys - 4 Methylationmethylation in fission yeast. |
| 0.5062 | Here we demonstrate that deletion of set1, which encodes a protein containing an RNA recognition motif at its amino terminus and a SET domain at the carboxy terminus, abolishes EntityH3 Lys - 4 methylation in fission yeast. |
| Score | Text |
|---|---|
| 0.9135 | Unlike in budding yeast, Set1 - mediated H3 Lys - 4 Methylationmethylation is not required for heterochromatin assembly at the silent mating - type region and centromeres in fission yeast. |
| 0.6949 | Unlike in budding yeast, CatalysisSet1 - mediated H3 Lys - 4 methylation is not required for heterochromatin assembly at the silent mating - type region and centromeres in fission yeast. |
| 0.6140 | Unlike in budding yeast, Set1 - mediated ProteinH3 Lys - 4 methylation is not required for heterochromatin assembly at the silent mating - type region and centromeres in fission yeast. |
| 0.5954 | Unlike in budding yeast, Set1 - mediated H3 EntityLys - 4 methylation is not required for heterochromatin assembly at the silent mating - type region and centromeres in fission yeast. |
| 0.4851 | Unlike in budding yeast, ProteinSet1 - mediated H3 Lys - 4 methylation is not required for heterochromatin assembly at the silent mating - type region and centromeres in fission yeast. |
| Unlike in budding yeast, ProteinSet1 - mediated H3 Lys - 4 methylation is not required for heterochromatin assembly at the silent mating - type region and centromeres in fission yeast. | |
| Score | Text |
|---|---|
| 0.9939 | Our analysis suggests that H3 Lys - 4 methylation is a stable Proteinhistone modification present throughout the cell cycle, including mitosis. |
| 0.9929 | Our analysis suggests that H3 Lys - 4 Methylationmethylation is a stable histone modification present throughout the cell cycle, including mitosis. |
| 0.9775 | Our analysis suggests that ProteinH3 Lys - 4 methylation is a stable histone modification present throughout the cell cycle, including mitosis. |
| 0.9744 | Our analysis suggests that H3 EntityLys - 4 methylation is a stable histone modification present throughout the cell cycle, including mitosis. |
| Score | Text |
|---|---|
| 0.9968 | The loss of H3 Lys - 4 methylation in Proteinset1Delta cells is correlated with a decrease in histone H3 acetylation levels, suggesting a mechanistic link between H3 Lys - 4 methylation and acetylation of the H3 tail. |
| 0.9868 | The loss of H3 Lys - 4 methylation in set1Delta cells is correlated with a decrease in histone H3 Acetylationacetylation levels, suggesting a mechanistic link between H3 Lys - 4 methylation and acetylation of the H3 tail. |
| 0.9852 | The loss of H3 Lys - 4 methylation in set1Delta cells is correlated with a decrease in histone H3 acetylation levels, suggesting a mechanistic link between H3 Lys - 4 methylation and acetylation of the ProteinH3 tail. |
| 0.9817 | The loss of H3 Lys - 4 Methylationmethylation in set1Delta cells is correlated with a decrease in histone H3 acetylation levels, suggesting a mechanistic link between H3 Lys - 4 methylation and acetylation of the H3 tail. |
| 0.9795 | The loss of H3 Lys - 4 methylation in set1Delta cells is correlated with a decrease in histone H3 acetylation levels, suggesting a mechanistic link between H3 Lys - 4 Methylationmethylation and acetylation of the H3 tail. |
| 0.9785 | The loss of H3 Lys - 4 methylation in set1Delta cells is correlated with a decrease in histone H3 acetylation levels, suggesting a mechanistic link between ProteinH3 Lys - 4 methylation and acetylation of the H3 tail. |
| 0.9783 | The loss of ProteinH3 Lys - 4 methylation in set1Delta cells is correlated with a decrease in histone H3 acetylation levels, suggesting a mechanistic link between H3 Lys - 4 methylation and acetylation of the H3 tail. |
| 0.9774 | The loss of H3 EntityLys - 4 methylation in set1Delta cells is correlated with a decrease in histone H3 acetylation levels, suggesting a mechanistic link between H3 Lys - 4 methylation and acetylation of the H3 tail. |
| 0.9662 | The loss of H3 Lys - 4 methylation in set1Delta cells is correlated with a decrease in histone H3 acetylation levels, suggesting a mechanistic link between H3 EntityLys - 4 methylation and acetylation of the H3 tail. |
| 0.9568 | The loss of H3 Lys - 4 methylation in set1Delta cells is correlated with a decrease in Proteinhistone H3 acetylation levels, suggesting a mechanistic link between H3 Lys - 4 methylation and acetylation of the H3 tail. |
| 0.9528 | The loss of H3 Lys - 4 methylation in set1Delta cells is correlated with a decrease in histone H3 acetylation levels, suggesting a mechanistic link between H3 Lys - 4 methylation and acetylation of the H3 Entitytail . |
| 0.9435 | The loss of H3 Lys - 4 methylation in set1Delta cells is correlated with a decrease in histone H3 acetylation levels, suggesting a mechanistic link between H3 Lys - 4 methylation and Acetylationacetylation of the H3 tail. |
| Score | Text |
|---|---|
| 0.9887 | We suggest that methylation of H3 Lys - 4 primarily acts in the maintenance of transcriptionally poised euchromatic domains, and that this modification is dispensable for heterochromatin formation in fission yeast, which instead utilizes H3 Lys - 9 Methylationmethylation . |
| 0.9856 | We suggest that methylation of H3 Lys - 4 primarily acts in the maintenance of transcriptionally poised euchromatic domains, and that this modification is dispensable for heterochromatin formation in fission yeast, which instead utilizes ProteinH3 Lys - 9 methylation. |
| 0.9843 | We suggest that Methylationmethylation of H3 Lys - 4 primarily acts in the maintenance of transcriptionally poised euchromatic domains, and that this modification is dispensable for heterochromatin formation in fission yeast, which instead utilizes H3 Lys - 9 methylation. |
| 0.9743 | We suggest that methylation of ProteinH3 Lys - 4 primarily acts in the maintenance of transcriptionally poised euchromatic domains, and that this modification is dispensable for heterochromatin formation in fission yeast, which instead utilizes H3 Lys - 9 methylation. |
| 0.9669 | We suggest that methylation of H3 EntityLys - 4 primarily acts in the maintenance of transcriptionally poised euchromatic domains, and that this modification is dispensable for heterochromatin formation in fission yeast, which instead utilizes H3 Lys - 9 methylation. |
| 0.9653 | We suggest that methylation of H3 Lys - 4 primarily acts in the maintenance of transcriptionally poised euchromatic domains, and that this modification is dispensable for heterochromatin formation in fission yeast, which instead utilizes H3 EntityLys - 9 methylation. |
| Score | Text |
|---|---|
| 0.9643 | Hypoxia - inducible factor asparaginyl hydroxylase Protein( FIH - 1 ) catalyses hydroxylation at the beta - carbon of asparagine - 803. |
| 0.6652 | ProteinHypoxia - inducible factor asparaginyl hydroxylase ( FIH - 1 ) catalyses hydroxylation at the beta - carbon of asparagine - 803. |
| Score | Text |
|---|---|
| 0.9913 | Asparagine - 803 in the C - terminal transactivation domain of human hypoxia - inducible factor ( HIF ) - 1 alpha - subunit is hydroxylated by factor inhibiting HIF - 1 ( FIH - 1 ) under normoxic conditions causing abrogation of the ProteinHIF - 1alpha / p300 interaction. |
| 0.9737 | EntityAsparagine - 803 in the C - terminal transactivation domain of human hypoxia - inducible factor ( HIF ) - 1 alpha - subunit is hydroxylated by factor inhibiting HIF - 1 ( FIH - 1 ) under normoxic conditions causing abrogation of the HIF - 1alpha / p300 interaction. |
| 0.9419 | Asparagine - 803 in the C - terminal transactivation domain of human hypoxia - inducible factor ( HIF ) - 1 alpha - subunit is hydroxylated by factor inhibiting HIF - 1 Protein( FIH - 1 ) under normoxic conditions causing abrogation of the HIF - 1alpha / p300 interaction. |
| 0.8053 | Asparagine - 803 in the C - terminal transactivation domain of human hypoxia - inducible factor ( HIF ) - 1 alpha - subunit is hydroxylated by Proteinfactor inhibiting HIF - 1 ( FIH - 1 ) under normoxic conditions causing abrogation of the HIF - 1alpha / p300 interaction. |
| 0.6968 | Asparagine - 803 in the C - terminal transactivation domain of human hypoxia - inducible factor ( HIF ) - 1 alpha - subunit is Hydroxylationhydroxylated by factor inhibiting HIF - 1 ( FIH - 1 ) under normoxic conditions causing abrogation of the HIF - 1alpha / p300 interaction. |
| 0.5802 | Asparagine - 803 in the C - terminal transactivation domain of human Proteinhypoxia - inducible factor ( HIF ) - 1 alpha - subunit is hydroxylated by factor inhibiting HIF - 1 ( FIH - 1 ) under normoxic conditions causing abrogation of the HIF - 1alpha / p300 interaction. |
| Asparagine - 803 in the C - terminal transactivation domain of human hypoxia - inducible factor ( HIF ) - 1 alpha - subunit is Catalysishydroxylated by factor inhibiting HIF - 1 ( FIH - 1 ) under normoxic conditions causing abrogation of the HIF - 1alpha / p300 interaction. | |
| Score | Text |
|---|---|
| 0.9586 | NMR and other analyses of a hydroxylated HIF fragment produced in vitro demonstrate that hydroxylation occurs at the beta - carbon of EntityAsn - 803 and imply production of the threo - isomer, in contrast with other known aspartic acid / asparagine hydroxylases that produce the erythro - isomer. |
| 0.9496 | NMR and other analyses of a hydroxylated HIF fragment produced in vitro demonstrate that Hydroxylationhydroxylation occurs at the beta - carbon of Asn - 803 and imply production of the threo - isomer, in contrast with other known aspartic acid / asparagine hydroxylases that produce the erythro - isomer. |
| 0.7227 | NMR and other analyses of a Hydroxylationhydroxylated HIF fragment produced in vitro demonstrate that hydroxylation occurs at the beta - carbon of Asn - 803 and imply production of the threo - isomer, in contrast with other known aspartic acid / asparagine hydroxylases that produce the erythro - isomer. |
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| 0.9986 | The activity of serum GOT, ProteinGPT and alkaline phosphatase was also unchanged. |
| 0.9984 | The activity of serum ProteinGOT , GPT and alkaline phosphatase was also unchanged. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
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|---|---|
| 0.9981 | CD437 and MM002 induce apoptosis in both cell lines, as indicated by the activation of caspase - 2 and Proteincaspase - 3 , cleavage of poly ( adenosine diphosphate - ribose ) ( poly ( ADP - ribose ) ) polymerase, increase in annexin V binding, and subsequent nuclear fragmentation. |
| 0.9964 | CD437 and MM002 induce apoptosis in both cell lines, as indicated by the activation of Proteincaspase - 2 and caspase - 3, cleavage of poly ( adenosine diphosphate - ribose ) ( poly ( ADP - ribose ) ) polymerase, increase in annexin V binding, and subsequent nuclear fragmentation. |
| 0.9861 | CD437 and MM002 induce apoptosis in both cell lines, as indicated by the activation of caspase - 2 and caspase - 3, cleavage of poly ( adenosine diphosphate - ribose ) ( poly ( ADP - ribose ) ) polymerase, increase in Proteinannexin V binding, and subsequent nuclear fragmentation. |
| Score | Text |
|---|---|
| 0.9996 | CD437 - mediated apoptosis was not associated with the modulation of ProteinBcl - 2 , Bax, or Mcl - 1 levels, but was associated with the cleavage of the antiapoptotic protein Bcl - X ( L ) to a proapoptotic 18 - kD form. |
| 0.9994 | CD437 - mediated apoptosis was not associated with the modulation of Bcl - 2, Bax, or ProteinMcl - 1 levels, but was associated with the cleavage of the antiapoptotic protein Bcl - X ( L ) to a proapoptotic 18 - kD form. |
| 0.9993 | CD437 - mediated apoptosis was not associated with the modulation of Bcl - 2, ProteinBax , or Mcl - 1 levels, but was associated with the cleavage of the antiapoptotic protein Bcl - X ( L ) to a proapoptotic 18 - kD form. |
| 0.9830 | CD437 - mediated apoptosis was not associated with the modulation of Bcl - 2, Bax, or Mcl - 1 levels, but was associated with the cleavage of the antiapoptotic protein ProteinBcl - X ( L ) to a proapoptotic 18 - kD form. |
| 0.6090 | ProteinCD437 - mediated apoptosis was not associated with the modulation of Bcl - 2, Bax, or Mcl - 1 levels, but was associated with the cleavage of the antiapoptotic protein Bcl - X ( L ) to a proapoptotic 18 - kD form. |
| Score | Text |
|---|---|
| 0.9979 | This cleavage of ProteinBcl - X ( L ) was dependent on caspase - 3 activation since Bcl - X ( L ) cleavage and apoptosis were inhibited by the caspase - 3 inhibitor Z - DVED - fmk. |
| 0.9970 | This cleavage of Bcl - X ( L ) was dependent on Proteincaspase - 3 activation since Bcl - X ( L ) cleavage and apoptosis were inhibited by the caspase - 3 inhibitor Z - DVED - fmk. |
| 0.9960 | This cleavage of Bcl - X ( L ) was dependent on caspase - 3 activation since ProteinBcl - X ( L ) cleavage and apoptosis were inhibited by the caspase - 3 inhibitor Z - DVED - fmk. |
| 0.9914 | This cleavage of Bcl - X ( L ) was dependent on caspase - 3 activation since Bcl - X ( L ) cleavage and apoptosis were inhibited by the Proteincaspase - 3 inhibitor Z - DVED - fmk. |
| Score | Text |
|---|---|
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| Score | Text |
|---|---|
| 0.9995 | The product of the von Hippel - Lindau gene, ProteinpVHL , targets the alpha subunits of the heterodimeric transcription factor hypoxia - inducible factor ( HIF ) for polyubiquitination in the presence of oxygen. |
| 0.5735 | The product of the Proteinvon Hippel - Lindau gene , pVHL, targets the alpha subunits of the heterodimeric transcription factor hypoxia - inducible factor ( HIF ) for polyubiquitination in the presence of oxygen. |
| 0.8365 | The product of the Proteinvon Hippel - Lindau gene, pVHL, targets the alpha subunits of the heterodimeric transcription factor hypoxia - inducible factor ( HIF ) for polyubiquitination in the presence of oxygen. |
| 0.6372 | The product of the von ProteinHippel - Lindau gene, pVHL, targets the alpha subunits of the heterodimeric transcription factor hypoxia - inducible factor ( HIF ) for polyubiquitination in the presence of oxygen. |
| 0.6196 | The product of the von Hippel - Lindau gene, pVHL, targets the alpha subunits of the heterodimeric transcription factor hypoxia - inducible factor ( HIF ) for Ubiquitinationpolyubiquitination in the presence of oxygen. |
| Score | Text |
|---|---|
| 0.9995 | The binding of ProteinpVHL to HIF is governed by the enzymatic hydroxylation of conserved prolyl residues within peptidic motifs present in the HIFalpha family members. |
| 0.6625 | The binding of pVHL to HIF is governed by the enzymatic Hydroxylationhydroxylation of conserved prolyl residues within peptidic motifs present in the HIFalpha family members. |
| Score | Text |
|---|---|
| 0.9993 | By using a biochemical purification strategy, we have identified a human homolog of Caenorhabditis elegans ProteinEgl9 as a HIF prolyl hydroxylase. |
| Score | Text |
|---|---|
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|---|---|
| 0.8641 | A model compound of this series stabilized HIF in a variety of cells, leading to the increased production of its downstream target, Proteinvascular endothelial growth factor . |
| 0.5768 | A model compound of this series stabilized HIF in a variety of cells, leading to the increased production of its downstream target, vascular Proteinendothelial growth factor . |
| Score | Text |
|---|---|
| 0.9573 | Control of CBP co - activating activity by arginine Methylationmethylation . |
| 0.9331 | Control of ProteinCBP co - activating activity by arginine methylation. |
| 0.9331 | Control of CBP co - activating activity by Entityarginine methylation. |
| Score | Text |
|---|---|
| 0.9977 | The histone acetyltransferases CREB binding protein ( CBP ) and the related Proteinp300 protein function as key transcriptional co - activators in multiple pathways. |
| 0.9973 | The Proteinhistone acetyltransferases CREB binding protein ( CBP ) and the related p300 protein function as key transcriptional co - activators in multiple pathways. |
| 0.9768 | The histone acetyltransferases CREB binding protein Protein( CBP ) and the related p300 protein function as key transcriptional co - activators in multiple pathways. |
| 0.8809 | The histone acetyltransferases ProteinCREB binding protein ( CBP ) and the related p300 protein function as key transcriptional co - activators in multiple pathways. |
| Score | Text |
|---|---|
| 0.9983 | In the case of transcriptional activation by nuclear receptors, ligand promotes the recruitment of co - activators of the p160 family, such as ProteinGRIP - 1 . |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9997 | AD1 binds CBP or p300, whereas AD2 has been shown to activate transcription through the recruitment of the arginine methyltransferase ProteinCARM1 . |
| 0.9996 | AD1 binds CBP or Proteinp300 , whereas AD2 has been shown to activate transcription through the recruitment of the arginine methyltransferase CARM1. |
| 0.9992 | AD1 binds ProteinCBP or p300, whereas AD2 has been shown to activate transcription through the recruitment of the arginine methyltransferase CARM1. |
| Score | Text |
|---|---|
| 0.9981 | Recently, the KIX domain of CBP has been shown to be methylated by ProteinCARM1 in vitro. |
| 0.9929 | Recently, the KIX domain of ProteinCBP has been shown to be methylated by CARM1 in vitro. |
| 0.7963 | Recently, the EntityKIX domain of CBP has been shown to be methylated by CARM1 in vitro. |
| 0.5521 | Recently, the KIX domain of CBP has been shown to be Catalysismethylated by CARM1 in vitro. |
| 0.5713 | Recently, the EntityKIX domain of CBP has been shown to be methylated by CARM1 in vitro. |
| Recently, the KIX domain of CBP has been shown to be Methylationmethylated by CARM1 in vitro. | |
| Score | Text |
|---|---|
| 0.9996 | Here, we report that another domain of ProteinCBP is specifically methylated by CARM1 on conserved arginine residues in vitro and in vivo. |
| 0.9994 | Here, we report that another domain of CBP is specifically methylated by ProteinCARM1 on conserved arginine residues in vitro and in vivo. |
| 0.5629 | Here, we report that another domain of CBP is specifically Catalysismethylated by CARM1 on conserved arginine residues in vitro and in vivo. |
| Here, we report that another domain of CBP is specifically Methylationmethylated by CARM1 on conserved arginine residues in vitro and in vivo. | |
| Score | Text |
|---|---|
| 0.9991 | We also provide functional evidence that arginine residues methylated by ProteinCARM1 play a critical role in GRIP - 1 - dependent transcriptional activation and in hormone - induced gene activation. |
| 0.9973 | We also provide functional evidence that arginine residues methylated by CARM1 play a critical role in ProteinGRIP - 1 - dependent transcriptional activation and in hormone - induced gene activation. |
| 0.8416 | We also provide functional evidence that Entityarginine residues methylated by CARM1 play a critical role in GRIP - 1 - dependent transcriptional activation and in hormone - induced gene activation. |
| 0.4810 | We also provide functional evidence that arginine residues Methylationmethylated by CARM1 play a critical role in GRIP - 1 - dependent transcriptional activation and in hormone - induced gene activation. |
| 0.7698 | We also provide functional evidence that Entityarginine residues methylated by CARM1 play a critical role in GRIP - 1 - dependent transcriptional activation and in hormone - induced gene activation. |
| We also provide functional evidence that arginine residues Catalysismethylated by CARM1 play a critical role in GRIP - 1 - dependent transcriptional activation and in hormone - induced gene activation. | |
| Score | Text |
|---|---|
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|---|---|
| 0.9200 | The hepatitis C virus ProteinRNA - dependent RNA polymerase membrane insertion sequence is a transmembrane segment. |
| 0.6697 | The hepatitis C virus RNA - dependent ProteinRNA polymerase membrane insertion sequence is a transmembrane segment. |
| Score | Text |
|---|---|
| 0.9795 | The hepatitis C virus ( HCV ) RNA - dependent RNA polymerase Protein( RdRp ) belongs to a class of membrane proteins termed tail - anchored proteins. |
| 0.8625 | The hepatitis C virus ( HCV ) ProteinRNA - dependent RNA polymerase ( RdRp ) belongs to a class of membrane proteins termed tail - anchored proteins. |
| Score | Text |
|---|---|
| 0.9999 | Here, we show that the HCV ProteinRdRp C - terminal membrane insertion sequence traverses the phospholipid bilayer as a transmembrane segment. |
| Score | Text |
|---|---|
| 0.9998 | Moreover, the HCV ProteinRdRp was found to be retained in the endoplasmic reticulum ( ER ) or an ER - derived modified compartment both following transient transfection and in the context of a subgenomic replicon. |
| Score | Text |
|---|---|
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|---|---|
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|---|---|
| 0.9678 | Molecular and biochemical characterisation of a novel sulphatase gene : Arylsulfatase G Protein( ARSG ) . |
| 0.8697 | Molecular and biochemical characterisation of a novel sulphatase gene : ProteinArylsulfatase G ( ARSG ). |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9786 | Through bioinformatic searches of the EST database, we have identified a novel gene consisting of 11 exons and encoding a 525 aa protein that shares a high degree of sequence similarity with all sulphatases and in particular with arylsulphatases, hence the tentative name Arylsulfatase G Protein( ARSG ) . |
| 0.9090 | Through bioinformatic searches of the EST database, we have identified a novel gene consisting of 11 exons and encoding a 525 aa protein that shares a high degree of sequence similarity with all sulphatases and in particular with arylsulphatases, hence the tentative name ProteinArylsulfatase G ( ARSG ). |
| Score | Text |
|---|---|
| 0.9628 | The highest homology is shared with ProteinArylsulfatase A , a lysosomal sulphatase which is mutated in metachromatic leukodistrophy, particularly in the amino - terminal region. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9778 | The murine homologue of ProteinArylsulfatase G gene product shows 87 % identity with the human protein. |
| Score | Text |
|---|---|
| 0.9556 | To test the function of this novel gene we transfected the full - length cDNA in Cos7 cells, and detected an ProteinArylsulfatase G precursor protein of 62 kDa. |
| Score | Text |
|---|---|
| 0.9557 | After Glycosylationglycosylation the precursor is maturated in a 70 kDa form, which localises to the endoplasmic reticulum. |
| Score | Text |
|---|---|
| 0.9614 | Northern blot analysis of ProteinArylsulfatase G revealed a ubiquitous expression pattern. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9161 | Further studies are needed to characterise the function of ProteinArylsulfatase G , possibly revealing a novel metabolic pathway. |
| Score | Text |
|---|---|
| 0.9915 | Gene - specific targeting of H3K9 Methylationmethylation is sufficient for initiating repression in vivo. |
| 0.4964 | Gene - specific targeting of EntityH3K9 methylation is sufficient for initiating repression in vivo. |
| Gene - specific targeting of ProteinH3K9 methylation is sufficient for initiating repression in vivo. | |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9796 | Histone H3 lysine 9 ( H3K9 ) Methylationmethylation is an epigenetic signal that is recognized by HP1 and correlates with gene silencing in a variety of organisms. |
| 0.8773 | Histone H3 Entitylysine 9 ( H3K9 ) methylation is an epigenetic signal that is recognized by HP1 and correlates with gene silencing in a variety of organisms. |
| 0.8742 | ProteinHistone H3 lysine 9 ( H3K9 ) methylation is an epigenetic signal that is recognized by HP1 and correlates with gene silencing in a variety of organisms. |
| 0.6420 | Histone H3 lysine 9 Protein( H3K9 ) methylation is an epigenetic signal that is recognized by HP1 and correlates with gene silencing in a variety of organisms. |
| Histone H3 lysine 9 Entity( H3K9 ) methylation is an epigenetic signal that is recognized by HP1 and correlates with gene silencing in a variety of organisms. | |
| Score | Text |
|---|---|
| 0.9932 | Discovery of the enzymes that catalyze H3K9 Methylationmethylation has identified a second gene - specific function for this modification in transcriptional repression. |
| 0.5202 | Discovery of the enzymes that catalyze EntityH3K9 methylation has identified a second gene - specific function for this modification in transcriptional repression. |
| Discovery of the enzymes that catalyze ProteinH3K9 methylation has identified a second gene - specific function for this modification in transcriptional repression. | |
| Score | Text |
|---|---|
| 0.9751 | Whether H3K9 Methylationmethylation is causative in the initiation and establishment of gene repression or is a byproduct of the process leading to the repressed state remains unknown. |
| 0.6680 | Whether EntityH3K9 methylation is causative in the initiation and establishment of gene repression or is a byproduct of the process leading to the repressed state remains unknown. |
| Whether ProteinH3K9 methylation is causative in the initiation and establishment of gene repression or is a byproduct of the process leading to the repressed state remains unknown. | |
| Score | Text |
|---|---|
| 0.9816 | To investigate the role of HMTs and specifically H3K9 Methylationmethylation in gene repression, we have employed engineered zinc - finger transcription factors ( ZFPs ) to target HMT activity to a specific endogenous gene. |
| 0.6073 | To investigate the role of HMTs and specifically EntityH3K9 methylation in gene repression, we have employed engineered zinc - finger transcription factors ( ZFPs ) to target HMT activity to a specific endogenous gene. |
| To investigate the role of HMTs and specifically ProteinH3K9 methylation in gene repression, we have employed engineered zinc - finger transcription factors ( ZFPs ) to target HMT activity to a specific endogenous gene. | |
| Score | Text |
|---|---|
| 0.9995 | By utilizing ZFPs that recognize the promoter of the endogenous ProteinVEGF - A gene, and thus employing this chromosomal locus as an in vivo reporter, we show that ZFPs linked to a minimal catalytic HMT domain affect local methylation of histone H3K9 and the consequent repression of target gene expression. |
| 0.9609 | By utilizing ZFPs that recognize the promoter of the endogenous VEGF - A gene, and thus employing this chromosomal locus as an in vivo reporter, we show that ZFPs linked to a minimal catalytic HMT domain affect local Methylationmethylation of histone H3K9 and the consequent repression of target gene expression. |
| 0.9582 | By utilizing ZFPs that recognize the promoter of the endogenous VEGF - A gene, and thus employing this chromosomal locus as an in vivo reporter, we show that ZFPs linked to a minimal catalytic HMT domain affect local methylation of histone EntityH3K9 and the consequent repression of target gene expression. |
| 0.5971 | By utilizing ZFPs that recognize the promoter of the endogenous VEGF - A gene, and thus employing this chromosomal locus as an in vivo reporter, we show that ZFPs linked to a minimal catalytic HMT domain affect local methylation of Proteinhistone H3K9 and the consequent repression of target gene expression. |
| 0.5517 | By utilizing ZFPs that recognize the Entitypromoter of the endogenous VEGF - A gene, and thus employing this chromosomal locus as an in vivo reporter, we show that ZFPs linked to a minimal catalytic HMT domain affect local methylation of histone H3K9 and the consequent repression of target gene expression. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9805 | Thus, H3K9 Methylationmethylation is a primary signal that is sufficient for initiating a gene repression pathway in vivo. |
| 0.6792 | Thus, EntityH3K9 methylation is a primary signal that is sufficient for initiating a gene repression pathway in vivo. |
| Thus, ProteinH3K9 methylation is a primary signal that is sufficient for initiating a gene repression pathway in vivo. | |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9998 | The majority of the SeCys conjugates produced near complete inhibition of ProteinCYP1A1 at a concentration of 250 microm. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9988 | CYP2C9, Protein- 2C19 and - 2D6 were moderately ( 50 - 60 % ) inhibited by the SeCys conjugates. |
| 0.9982 | CYP2C9, - 2C19 and Protein- 2D6 were moderately ( 50 - 60 % ) inhibited by the SeCys conjugates. |
| 0.9980 | ProteinCYP2C9 , - 2C19 and - 2D6 were moderately ( 50 - 60 % ) inhibited by the SeCys conjugates. |
| Score | Text |
|---|---|
| 0.9986 | CYP1A2, Protein- 2E1 and - 3A4 were least inhibited. 3. |
| 0.9985 | ProteinCYP1A2 , - 2E1 and - 3A4 were least inhibited. 3. |
| 0.9975 | CYP1A2, - 2E1 and Protein- 3A4 were least inhibited. 3. |
| Score | Text |
|---|---|
| 0.9998 | Studies on the susceptibility of ProteinCYP1A1 to SeCys conjugates implicated a thiol - reactive intermediate, as evidenced by reduced inhibition levels in the presence of glutathione and N - acetyl cysteine. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9974 | N - acetylation of SeCys conjugates consistently increased the inhibitory potency towards CYP1A2, - 2C19, - 2E1 and Protein- 3A4 . |
| 0.9970 | N - acetylation of SeCys conjugates consistently increased the inhibitory potency towards CYP1A2, - 2C19, Protein- 2E1 and - 3A4. |
| 0.9967 | N - acetylation of SeCys conjugates consistently increased the inhibitory potency towards ProteinCYP1A2 , - 2C19, - 2E1 and - 3A4. |
| 0.9956 | N - acetylation of SeCys conjugates consistently increased the inhibitory potency towards CYP1A2, Protein- 2C19 , - 2E1 and - 3A4. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9997 | It is concluded that the potent and relatively selective ProteinCYP1A1 inhibition exerted by SeCys conjugates may contribute to their chemopreventive activity. |
| Score | Text |
|---|---|
| 0.9988 | Identification of a lactoferrin - derived peptide possessing binding activity to hepatitis C virus ProteinE2 envelope protein. |
| 0.9945 | Identification of a Proteinlactoferrin - derived peptide possessing binding activity to hepatitis C virus E2 envelope protein. |
| Score | Text |
|---|---|
| 0.9995 | Bovine and human lactoferrins ( LF ) prevent hepatitis C virus ( HCV ) infection in cultured human hepatocytes ; the preventive mechanism is thought to be the direct interaction between ProteinLF and HCV. |
| 0.9830 | Bovine and human lactoferrins Protein( LF ) prevent hepatitis C virus ( HCV ) infection in cultured human hepatocytes ; the preventive mechanism is thought to be the direct interaction between LF and HCV. |
| 0.9812 | Bovine and human Proteinlactoferrins ( LF ) prevent hepatitis C virus ( HCV ) infection in cultured human hepatocytes ; the preventive mechanism is thought to be the direct interaction between LF and HCV. |
| Score | Text |
|---|---|
| 0.9979 | To clarify this hypothesis, we have characterized the binding activity of LF to HCV ProteinE2 envelope protein and have endeavored to determine which region ( s ) of LF are important for this binding activity. |
| 0.9955 | To clarify this hypothesis, we have characterized the binding activity of ProteinLF to HCV E2 envelope protein and have endeavored to determine which region ( s ) of LF are important for this binding activity. |
| 0.9952 | To clarify this hypothesis, we have characterized the binding activity of LF to HCV E2 envelope protein and have endeavored to determine which region ( s ) of ProteinLF are important for this binding activity. |
| Score | Text |
|---|---|
| 0.9994 | Several regions of human ProteinLF have been expressed and purified as thioredoxin - fused proteins in Escherichia coli. |
| Score | Text |
|---|---|
| 0.9996 | Far - Western blot analysis using these LF fragments and the E2 protein, expressed in Chinese hamster ovary cells, revealed that the 93 carboxyl amino acids of ProteinLF specifically bound to the E2 protein. |
| 0.9995 | Far - Western blot analysis using these LF fragments and the ProteinE2 protein, expressed in Chinese hamster ovary cells, revealed that the 93 carboxyl amino acids of LF specifically bound to the E2 protein. |
| 0.9993 | Far - Western blot analysis using these LF fragments and the E2 protein, expressed in Chinese hamster ovary cells, revealed that the 93 carboxyl amino acids of LF specifically bound to the ProteinE2 protein. |
| 0.9976 | Far - Western blot analysis using these ProteinLF fragments and the E2 protein, expressed in Chinese hamster ovary cells, revealed that the 93 carboxyl amino acids of LF specifically bound to the E2 protein. |
| Score | Text |
|---|---|
| 0.9996 | The 93 carboxyl amino acids of ProteinLFs derived from bovine and horse cells also possessed similar binding activity to the E2 protein. |
| 0.9995 | The 93 carboxyl amino acids of LFs derived from bovine and horse cells also possessed similar binding activity to the ProteinE2 protein. |
| Score | Text |
|---|---|
| 0.9996 | In addition, the amino acid sequences of these carboxyl regions appeared to show partial homology to ProteinCD81 , a candidate receptor for HCV, and the binding activity of these carboxyl regions was also comparable with that of CD81. |
| 0.9993 | In addition, the amino acid sequences of these carboxyl regions appeared to show partial homology to CD81, a candidate receptor for HCV, and the binding activity of these carboxyl regions was also comparable with that of ProteinCD81 . |
| Score | Text |
|---|---|
| 0.9982 | Further deletion analysis identified 33 amino acid residues as the minimum binding site in the carboxyl region of ProteinLF , and the binding specificity of these 33 amino acids was also confirmed by using 33 maltose - binding protein - fused amino acids. |
| Score | Text |
|---|---|
| 0.9200 | Furthermore, we demonstrated that the 33 Proteinmaltose - binding protein - fused amino acids prevented HCV infection in cultured human hepatocytes. |
| Score | Text |
|---|---|
| 0.9994 | In addition, the site - directed mutagenesis to an Ala residue in both terminal residues of the 33 amino acids revealed that Cys at amino acid 628 was determined to be critical for binding to the ProteinE2 protein. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9992 | This is the first identification of a natural protein - derived peptide that specifically binds to HCV ProteinE2 protein and prevents HCV infection. |
| Score | Text |
|---|---|
| 0.9970 | Glucocorticoid suppression of nuclear factor - kappa B : a role for Proteinhistone modifications. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9980 | These bind to, and activate, co - activator molecules that then acetylate core Proteinhistones resulting in elevated gene transcription. |
| 0.9838 | These bind to, and activate, co - activator molecules that then Acetylationacetylate core histones resulting in elevated gene transcription. |
| Score | Text |
|---|---|
| 0.9993 | Corticosteroids reverse histone acetylation at the site of inflammatory gene transcription, either by direct binding of the activated glucocorticoid receptor to NF - kappa B - associated co - activators or by recruitment of Proteinhistone deacetylases to the activated transcription complex. |
| 0.9971 | Corticosteroids reverse Proteinhistone acetylation at the site of inflammatory gene transcription, either by direct binding of the activated glucocorticoid receptor to NF - kappa B - associated co - activators or by recruitment of histone deacetylases to the activated transcription complex. |
| 0.9951 | Corticosteroids reverse histone Acetylationacetylation at the site of inflammatory gene transcription, either by direct binding of the activated glucocorticoid receptor to NF - kappa B - associated co - activators or by recruitment of histone deacetylases to the activated transcription complex. |
| 0.9606 | Corticosteroids reverse histone acetylation at the site of inflammatory gene transcription, either by direct binding of the activated Proteinglucocorticoid receptor to NF - kappa B - associated co - activators or by recruitment of histone deacetylases to the activated transcription complex. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9929 | Probing the conformational and dynamical effects of O - glycosylation within the immunodominant region of a ProteinMUC1 peptide tumor antigen. |
| 0.9927 | Probing the conformational and dynamical effects of GlycosylationO - glycosylation within the immunodominant region of a MUC1 peptide tumor antigen. |
| 0.7962 | Probing the conformational and dynamical effects of O - glycosylation within the Entityimmunodominant region of a MUC1 peptide tumor antigen. |
| Score | Text |
|---|---|
| 0.9826 | ProteinMUC1 mucin is a large transmembrane glycoprotein, the extracellular domain of which is formed by a repeating 20 amino acid sequence, GVTSAPDTRPAPGSTAPPAH. |
| 0.5706 | MUC1 mucin is a large transmembrane glycoprotein, the extracellular domain of which is formed by a repeating 20 amino acid sequence, ProteinGVTSAPDTRPAPGSTAPPAH . |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9895 | However, in neoplastic breast tissue, the extracellular domain is Glycosylationunder - glycosylated , resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates. |
| 0.9833 | However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core EntityTn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates. |
| 0.9695 | However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), EntitySTn ( sialyl alpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates. |
| 0.9624 | However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and EntityTF ( Gal beta1 - 3 GalNAc ) carbohydrates. |
| 0.9619 | However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn Entity( GalNAc ) , STn ( sialyl alpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates. |
| 0.8804 | However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and TF Entity( Gal beta1 - 3 GalNAc ) carbohydrates. |
| 0.8337 | However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn Entity( sialyl alpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates. |
| 0.9785 | However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 EntityGalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates. |
| 0.9575 | However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 EntityGalNAc ) carbohydrates. |
| 0.9523 | However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core EntityTn ( GalNAc ) , STn ( sialyl alpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates. |
| 0.9232 | However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl Entityalpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates. |
| 0.9076 | However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and TF ( Gal Entitybeta1 - 3 GalNAc ) carbohydrates. |
| 0.8761 | However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and EntityTF ( Gal beta1 - 3 GalNAc ) carbohydrates. |
| 0.8266 | However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), EntitySTn ( sialyl alpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates. |
| 0.7873 | However, in neoplastic breast tissue, the extracellular Entitydomain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates. |
| 0.7721 | However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl Entityalpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates. |
| 0.7588 | However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and EntityTF ( Gal beta1 - 3 GalNAc ) carbohydrates. |
| 0.7582 | However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and TF ( Gal Entitybeta1 - 3 GalNAc ) carbohydrates. |
| 0.7263 | However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and TF Entity( Gal beta1 - 3 GalNAc ) carbohydrates. |
| 0.7236 | However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and EntityTF ( Gal beta1 - 3 GalNAc ) carbohydrates. |
| 0.6652 | However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), EntitySTn ( sialyl alpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates. |
| 0.6415 | However, in neoplastic breast tissue, the Glycosylationextracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates. |
| 0.6345 | However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and TF Entity( Gal beta1 - 3 GalNAc ) carbohydrates. |
| 0.6316 | However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn Entity( sialyl alpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates. |
| 0.6209 | However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), EntitySTn ( sialyl alpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates. |
| 0.5170 | However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 EntityGalNAc ) carbohydrates . |
| However, in neoplastic breast tissue, the Entityextracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates. | |
| Score | Text |
|---|---|
| 0.6019 | Here, we report the results of 1H NMR structural studies, natural abundance 13C NMR relaxation measurements and distance - restrained MD simulations designed to probe the structural and dynamical effects of GlycosylationTn - glycosylation within the PDTRP core peptide epitope. |
| Score | Text |
|---|---|
| 0.9968 | Two synthetic peptides were studied : a nine - residue ProteinMUC1 peptide of the sequence, Thr1 - Ser2 - Ala3 - Pro4 - Asp5 - Thr6 - Arg7 - Pro8 - Ala9, and a Tn - glycosylated version of this peptide, Thr1 - Ser2 - Ala3 - Pro4 - Asp5 - Thr6 ( alphaGalNAc ) - Arg7 - Pro8 - Ala9. |
| 0.9156 | Two synthetic peptides were studied : a nine - residue MUC1 peptide of the sequence, Thr1 - Ser2 - Ala3 - Pro4 - Asp5 - Thr6 - Arg7 - Pro8 - Ala9, and a GlycosylationTn - glycosylated version of this peptide, Thr1 - Ser2 - Ala3 - Pro4 - Asp5 - Thr6 ( alphaGalNAc ) - Arg7 - Pro8 - Ala9. |
| 0.6593 | Two synthetic peptides were studied : a nine - residue MUC1 peptide of the sequence, EntityThr1 - Ser2 - Ala3 - Pro4 - Asp5 - Thr6 - Arg7 - Pro8 - Ala9 , and a Tn - glycosylated version of this peptide, Thr1 - Ser2 - Ala3 - Pro4 - Asp5 - Thr6 ( alphaGalNAc ) - Arg7 - Pro8 - Ala9. |
| Score | Text |
|---|---|
| 0.9973 | The results of these studies show that a type I beta - turn conformation is adopted by residues PDTR within the PDTRP region of the unglycosylated ProteinMUC1 sequence. |
| 0.9303 | The results of these studies show that a type I beta - turn conformation is adopted by residues PDTR within the PDTRP region of the Glycosylationunglycosylated MUC1 sequence. |
| Score | Text |
|---|---|
| 0.9935 | The existence of a similar beta - turn within the PDTRP core peptide epitope of the Glycosylationunder - glycosylated cancer - associated MUC1 mucin protein might explain the immunodominance of this region in vivo, as the presence of defined secondary structure within peptide epitope regions has been correlated with increased immunogenicity in other systems. |
| 0.9255 | The existence of a similar beta - turn within the PDTRP core peptide epitope of the under - glycosylated cancer - associated ProteinMUC1 mucin protein might explain the immunodominance of this region in vivo, as the presence of defined secondary structure within peptide epitope regions has been correlated with increased immunogenicity in other systems. |
| 0.7533 | The existence of a similar beta - turn within the PDTRP core peptide Entityepitope of the under - glycosylated cancer - associated MUC1 mucin protein might explain the immunodominance of this region in vivo, as the presence of defined secondary structure within peptide epitope regions has been correlated with increased immunogenicity in other systems. |
| The existence of a similar beta - turn within the EntityPDTRP core peptide epitope of the under - glycosylated cancer - associated MUC1 mucin protein might explain the immunodominance of this region in vivo, as the presence of defined secondary structure within peptide epitope regions has been correlated with increased immunogenicity in other systems. | |
| Score | Text |
|---|---|
| 0.8089 | Our results have also shown that Tn Glycosylationglycosylation at the central threonine within the PDTRP core epitope region shifts the conformational equilibrium away from the type I beta - turn conformation and toward a more rigid and extended state. |
| Score | Text |
|---|---|
| 0.9996 | The significance of these results are discussed in relation to the possible roles that peptide epitope secondary structure and glycosylation state may play in ProteinMUC1 tumor immunogenicity. |
| 0.9714 | The significance of these results are discussed in relation to the possible roles that peptide epitope secondary structure and Glycosylationglycosylation state may play in MUC1 tumor immunogenicity. |
| Score | Text |
|---|---|
| 0.9743 | EntityLysine - 79 of histone H3 is hypomethylated at silenced loci in yeast and mammalian cells : a potential mechanism for position - effect variegation. |
| 0.9735 | Lysine - 79 of histone H3 is Methylationhypomethylated at silenced loci in yeast and mammalian cells : a potential mechanism for position - effect variegation. |
| 0.9558 | Lysine - 79 of Proteinhistone H3 is hypomethylated at silenced loci in yeast and mammalian cells : a potential mechanism for position - effect variegation. |
| Score | Text |
|---|---|
| 0.9465 | Methylation of lysine - 79 ( K79 ) within the globular domain of Proteinhistone H3 by Dot1 methylase is important for transcriptional silencing and for association of the Sir silencing proteins in yeast. |
| 0.9322 | Methylation of lysine - 79 ( K79 ) within the globular domain of histone H3 by ProteinDot1 methylase is important for transcriptional silencing and for association of the Sir silencing proteins in yeast. |
| 0.9133 | Methylation of lysine - 79 Entity( K79 ) within the globular domain of histone H3 by Dot1 methylase is important for transcriptional silencing and for association of the Sir silencing proteins in yeast. |
| 0.8890 | Methylation of Entitylysine - 79 ( K79 ) within the globular domain of histone H3 by Dot1 methylase is important for transcriptional silencing and for association of the Sir silencing proteins in yeast. |
| 0.7087 | MethylationMethylation of lysine - 79 ( K79 ) within the globular domain of histone H3 by Dot1 methylase is important for transcriptional silencing and for association of the Sir silencing proteins in yeast. |
| CatalysisMethylation of lysine - 79 ( K79 ) within the globular domain of histone H3 by Dot1 methylase is important for transcriptional silencing and for association of the Sir silencing proteins in yeast. | |
| Score | Text |
|---|---|
| 0.9696 | Here, we show that the level of H3 - K79 Methylationmethylation is low at all Sir - dependent silenced loci but not at other transcriptionally repressed regions. |
| 0.4977 | Here, we show that the level of EntityH3 - K79 methylation is low at all Sir - dependent silenced loci but not at other transcriptionally repressed regions. |
| Here, we show that the level of ProteinH3 - K79 methylation is low at all Sir - dependent silenced loci but not at other transcriptionally repressed regions. | |
| Score | Text |
|---|---|
| 0.8828 | MethylationHypomethylation of H3 - K79 at the telomeric and silent mating - type loci, but not the ribosomal DNA, requires the Sir proteins. |
| 0.5668 | Hypomethylation of ProteinH3 - K79 at the telomeric and silent mating - type loci, but not the ribosomal DNA, requires the Sir proteins. |
| Hypomethylation of EntityH3 - K79 at the telomeric and silent mating - type loci, but not the ribosomal DNA, requires the Sir proteins. | |
| Score | Text |
|---|---|
| 0.9980 | Overexpression of ProteinSir3 concomitantly extends the domain of Sir protein association and H3 - K79 hypomethylation at telomeres. |
| 0.9036 | Overexpression of Sir3 concomitantly extends the domain of Sir protein association and H3 - K79 Methylationhypomethylation at telomeres. |
| 0.6012 | Overexpression of Sir3 concomitantly extends the domain of Sir protein association and EntityH3 - K79 hypomethylation at telomeres. |
| Overexpression of Sir3 concomitantly extends the domain of Sir protein association and ProteinH3 - K79 hypomethylation at telomeres. | |
| Score | Text |
|---|---|
| 0.9888 | In mammalian cells, H3 - K79 Methylationmethylation is found at loci that are active for V ( D ) J recombination, but not at recombinationally inactive loci that are heterochromatic. |
| 0.5263 | In mammalian cells, EntityH3 - K79 methylation is found at loci that are active for V ( D ) J recombination, but not at recombinationally inactive loci that are heterochromatic. |
| In mammalian cells, ProteinH3 - K79 methylation is found at loci that are active for V ( D ) J recombination, but not at recombinationally inactive loci that are heterochromatic. | |
| Score | Text |
|---|---|
| 0.9973 | These results suggest that H3 - K79 methylation is an evolutionarily conserved marker of active chromatin regions, and that silencing proteins block the ability of ProteinDot1 to methylate histone H3. |
| 0.9796 | These results suggest that H3 - K79 Methylationmethylation is an evolutionarily conserved marker of active chromatin regions, and that silencing proteins block the ability of Dot1 to methylate histone H3. |
| 0.9361 | These results suggest that H3 - K79 methylation is an evolutionarily conserved marker of active chromatin regions, and that silencing proteins block the ability of Dot1 to methylate Proteinhistone H3 . |
| 0.9027 | These results suggest that H3 - K79 methylation is an evolutionarily conserved marker of active chromatin regions, and that silencing proteins block the ability of Dot1 to Methylationmethylate histone H3. |
| 0.5730 | These results suggest that ProteinH3 - K79 methylation is an evolutionarily conserved marker of active chromatin regions, and that silencing proteins block the ability of Dot1 to methylate histone H3. |
| These results suggest that EntityH3 - K79 methylation is an evolutionarily conserved marker of active chromatin regions, and that silencing proteins block the ability of Dot1 to methylate histone H3. | |
| These results suggest that H3 - K79 methylation is an evolutionarily conserved marker of active chromatin regions, and that silencing proteins block the ability of Dot1 to Catalysismethylate histone H3. | |
| Score | Text |
|---|---|
| 0.9930 | Further, they suggest that Sir proteins preferentially bind chromatin with hypomethylated H3 - K79 and then block H3 - K79 Methylationmethylation . |
| 0.9891 | Further, they suggest that Sir proteins preferentially bind chromatin with Methylationhypomethylated H3 - K79 and then block H3 - K79 methylation. |
| 0.5344 | Further, they suggest that Sir proteins preferentially bind chromatin with hypomethylated EntityH3 - K79 and then block H3 - K79 methylation. |
| 0.5262 | Further, they suggest that Sir proteins preferentially bind chromatin with hypomethylated H3 - K79 and then block EntityH3 - K79 methylation. |
| Further, they suggest that Sir proteins preferentially bind chromatin with hypomethylated ProteinH3 - K79 and then block H3 - K79 methylation. | |
| Further, they suggest that Sir proteins preferentially bind chromatin with hypomethylated H3 - K79 and then block ProteinH3 - K79 methylation. | |
| Score | Text |
|---|---|
| 0.9815 | This positive feedback loop, and the reverse loop in which H3 - K79 Methylationmethylation weakens Sir protein association and leads to further methylation, suggests a model for position - effect variegation. |
| 0.4951 | This positive feedback loop, and the reverse loop in which ProteinH3 - K79 methylation weakens Sir protein association and leads to further methylation, suggests a model for position - effect variegation. |
| This positive feedback loop, and the reverse loop in which EntityH3 - K79 methylation weakens Sir protein association and leads to further methylation, suggests a model for position - effect variegation. | |
| Score | Text |
|---|---|
| 0.9717 | Cyclosporin A prevents the hypoxic adaptation by activating hypoxia - inducible factor - 1alpha EntityPro - 564 hydroxylation. |
| 0.9477 | Cyclosporin A prevents the hypoxic adaptation by activating hypoxia - inducible factor - 1alpha Pro - 564 Hydroxylationhydroxylation . |
| 0.6583 | Cyclosporin A prevents the hypoxic adaptation by activating Proteinhypoxia - inducible factor - 1alpha Pro - 564 hydroxylation. |
| Score | Text |
|---|---|
| 0.9987 | The mechanism by which hypoxia induces gene transcription involves the inhibition of hypoxia - inducible factor ( HIF ) - 1alpha prolyl hydroxylase activity, which prevents von Hippel - Lindau ( vHL ) - dependent targeting of ProteinHIF - 1alpha to the ubiquitin - proteasome pathway. |
| 0.9985 | The mechanism by which hypoxia induces gene transcription involves the inhibition of hypoxia - inducible factor ( HIF ) - 1alpha prolyl hydroxylase activity, which prevents von Hippel - Lindau ( vHL ) - dependent targeting of HIF - 1alpha to the Proteinubiquitin - proteasome pathway. |
| 0.9351 | The mechanism by which hypoxia induces gene transcription involves the inhibition of hypoxia - inducible factor ( HIF ) - 1alpha prolyl hydroxylase activity, which prevents von Hippel - Lindau Protein( vHL ) - dependent targeting of HIF - 1alpha to the ubiquitin - proteasome pathway. |
| 0.6907 | The mechanism by which hypoxia induces gene transcription involves the inhibition of hypoxia - inducible factor ( HIF ) - 1alpha prolyl hydroxylase activity, which prevents Proteinvon Hippel - Lindau ( vHL ) - dependent targeting of HIF - 1alpha to the ubiquitin - proteasome pathway. |
| 0.5809 | The mechanism by which hypoxia induces gene transcription involves the inhibition of Proteinhypoxia - inducible factor ( HIF ) - 1alpha prolyl hydroxylase activity, which prevents von Hippel - Lindau ( vHL ) - dependent targeting of HIF - 1alpha to the ubiquitin - proteasome pathway. |
| The mechanism by which hypoxia induces gene transcription involves the inhibition of Proteinhypoxia - inducible factor ( HIF ) - 1alpha prolyl hydroxylase activity, which prevents von Hippel - Lindau ( vHL ) - dependent targeting of HIF - 1alpha to the ubiquitin - proteasome pathway. | |
| Score | Text |
|---|---|
| 0.9991 | ProteinHIF - 1alpha is stabilized, translocates to the nucleus, interacts with hypoxia - responsive elements, and promotes the activation of target genes. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9979 | CsA inhibits hypoxia - dependent gene transcription in a reporter gene assay and prevents the hypoxic accumulation of ProteinHIF - 1alpha . |
| Score | Text |
|---|---|
| 0.9992 | Addition of the 530 - 603 C - terminal oxygen - dependent degradation ( ODD ) domain of ProteinHIF - 1alpha to the green fluorescent protein ( GFP ) destabilized the protein in an oxygen - dependent manner. |
| 0.9878 | Addition of the 530 - 603 C - terminal oxygen - dependent degradation ( ODD ) domain of HIF - 1alpha to the green fluorescent protein Protein( GFP ) destabilized the protein in an oxygen - dependent manner. |
| 0.9178 | Addition of the 530 - 603 C - terminal oxygen - dependent degradation ( ODD ) domain of HIF - 1alpha to the Proteingreen fluorescent protein ( GFP ) destabilized the protein in an oxygen - dependent manner. |
| 0.6449 | Addition of the 530 - 603 C - terminal oxygen - dependent degradation ( ODD ) domain of HIF - 1alpha to the green Proteinfluorescent protein ( GFP ) destabilized the protein in an oxygen - dependent manner. |
| Score | Text |
|---|---|
| 0.9812 | CsA prevented the hypoxic stabilization of an ODD Protein. GFP fusion protein. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9990 | CsA stimulated the enzymatic activity in the presence of a peptide that mimicked the 557 - 576 sequence of ProteinHIF - 1alpha . |
| Score | Text |
|---|---|
| 0.9857 | The enzyme promoted Protein[ ( 35 ) S ] vHL binding to glutathione S - transferase ( GST ). ODD fusion protein. |
| 0.6056 | The enzyme promoted [ ( 35 ) S ] vHL binding to Proteinglutathione S - transferase ( GST ). ODD fusion protein. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9991 | CsA effects were not observed when the proline residue corresponding to Pro - 564 in the ProteinHIF - 1alpha sequence was replaced by a hydroxyproline or an alanine residue. |
| Score | Text |
|---|---|
| 0.9988 | Finally, CsA increased ProteinvHL - ODD interaction during hypoxia. |
| Score | Text |
|---|---|
| 0.9986 | We conclude that CsA destabilizes ProteinHIF - 1alpha by promoting hydroxylation of Pro - 564 in the ODD domain. |
| 0.9597 | We conclude that CsA destabilizes HIF - 1alpha by promoting Hydroxylationhydroxylation of Pro - 564 in the ODD domain. |
| 0.9593 | We conclude that CsA destabilizes HIF - 1alpha by promoting hydroxylation of EntityPro - 564 in the ODD domain. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9995 | A gene encoding a yeast peptide : N - glycanase, ProteinPNG1 , has been cloned, but this N - glycanase and its mammalian homolog were reported to be incapable of deglycosylating full - length glycoproteins. |
| Score | Text |
|---|---|
| 0.9996 | We show that both the yeast ProteinPNG1 enzyme and its mammalian homolog display N - glycanase activity towards intact glycoproteins. |
| Score | Text |
|---|---|
| 0.9987 | As substrates, cytosolic ProteinPNGase activity prefers proteins containing high - mannose over those bearing complex type oligosaccharides. |
| Score | Text |
|---|---|
| 0.9999 | Importantly, ProteinPNG1 discriminates between non - native and folded glycoproteins, consistent with a role for N - glycanase in cytoplasmic turnover of glycoproteins. |
| Score | Text |
|---|---|
| 0.9984 | Preclinical evaluation of antineoplastic activity of inhibitors of DNA methylation ( 5 - aza - 2'- deoxycytidine ) and Proteinhistone deacetylation ( trichostatin A, depsipeptide ) in combination against myeloid leukemic cells. |
| 0.8599 | Preclinical evaluation of antineoplastic activity of inhibitors of DNA methylation ( 5 - aza - 2'- deoxycytidine ) and histone Deacetylationdeacetylation ( trichostatin A, depsipeptide ) in combination against myeloid leukemic cells. |
| Score | Text |
|---|---|
| 0.9967 | During the development of leukemia, genes that suppress growth and induce differentiation can be silenced by aberrant DNA methylation and by changes in chromatin structure that involve Proteinhistone deacetylation. |
| 0.9130 | During the development of leukemia, genes that suppress growth and induce differentiation can be silenced by aberrant DNA methylation and by changes in chromatin structure that involve histone Deacetylationdeacetylation . |
| Score | Text |
|---|---|
| 0.9962 | It has been reported that a positive interaction between DNA methylation and Proteinhistone deacetylation takes place to inhibit transcription. |
| 0.8901 | It has been reported that a positive interaction between DNA methylation and histone Deacetylationdeacetylation takes place to inhibit transcription. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9993 | ProteinHistone deacetylase inhibitors ( HDI ) can also activate gene expression in leukemic cell lines by producing changes in chromatin configuration, and show antineoplastic activity in preclinical studies. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9931 | Complex - type biantennary N - glycans of recombinant human Proteintransferrin from Trichoplusia ni insect cells expressing mammalian [ beta ] - 1, 4 - galactosyltransferase and [ beta ] - 1, 2 - N - acetylglucosaminyltransferase II. |
| 0.5402 | Complex - type biantennary N - glycans of recombinant human transferrin from Trichoplusia ni insect cells expressing mammalian [ beta ] - 1, 4 - galactosyltransferase and Protein[ beta ] - 1, 2 - N - acetylglucosaminyltransferase II . |
| 0.6196 | Complex - type biantennary N - glycans of recombinant human transferrin from Trichoplusia ni insect cells expressing mammalian [ beta ] - 1, 4 - galactosyltransferase and [ beta ] - 1 Protein, 2 - N - acetylglucosaminyltransferase II . |
| Score | Text |
|---|---|
| 0.9994 | A novel recombinant baculovirus expression vector was used to produce His - tagged human Proteintransferrin in a transformed insect cell line ( Tn5beta4GalT ) that constitutively expresses a mammalian beta - 1, 4 - galactosyltransferase. |
| 0.7021 | A novel recombinant baculovirus expression vector was used to produce His - tagged human transferrin in a transformed insect cell line Protein( Tn5beta4GalT ) that constitutively expresses a mammalian beta - 1, 4 - galactosyltransferase. |
| Score | Text |
|---|---|
| 0.9981 | This virus encoded the His - tagged human Proteintransferrin protein in conventional fashion under the control of the very late polyhedrin promoter. |
| 0.9892 | This virus encoded the His - tagged human transferrin protein in conventional fashion under the control of the very late Proteinpolyhedrin promoter. |
| Score | Text |
|---|---|
| 0.9649 | In addition, to enhance the synthesis of galactosylated biantennary N - glycans, this virus encoded human beta - 1, 2 - N - acetylglucosaminyltransferase II under the control of an immediate - early Protein( ie1 ) promoter. |
| 0.5298 | In addition, to enhance the synthesis of galactosylated biantennary N - glycans, this virus encoded human Proteinbeta - 1, 2 - N - acetylglucosaminyltransferase II under the control of an immediate - early ( ie1 ) promoter. |
| 0.6877 | In addition, to enhance the synthesis of galactosylated biantennary N - glycans, this virus encoded human beta - 1, 2 - ProteinN - acetylglucosaminyltransferase II under the control of an immediate - early ( ie1 ) promoter. |
| 0.5578 | In addition, to enhance the synthesis of galactosylated biantennary N - glycans, this virus encoded human beta - 1 Protein, 2 - N - acetylglucosaminyltransferase II under the control of an immediate - early ( ie1 ) promoter. |
| Score | Text |
|---|---|
| 0.9988 | Detailed analyses by MALDI - TOF MS, exoglycosidase digestion, and two - dimensional HPLC revealed that the N - glycans on the purified recombinant human Proteintransferrin produced by this virus - host system included four different fully galactosylated, biantennary, complex - type glycans. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9169 | Overexpression of the ProteinCT GalNAc transferase inhibits muscular dystrophy in a cleavage - resistant dystroglycan mutant mouse. |
| 0.5200 | Overexpression of the CT ProteinGalNAc transferase inhibits muscular dystrophy in a cleavage - resistant dystroglycan mutant mouse. |
| Score | Text |
|---|---|
| 0.9982 | Transgenic mice that express Proteindystroglycan containing a serine to alanine point mutation at the normal site of cleavage ( DG ( S654A ) ) in their skeletal muscles fail to express endogenously cleaved dystroglycan and have muscular dystrophy [ Neuromusc. |
| 0.9977 | Transgenic mice that express dystroglycan containing a serine to alanine point mutation at the normal site of cleavage ( DG ( S654A ) ) in their skeletal muscles fail to express endogenously cleaved Proteindystroglycan and have muscular dystrophy [ Neuromusc. |
| 0.9892 | Transgenic mice that express dystroglycan containing a serine to alanine point mutation at the normal site of cleavage Protein( DG ( S654A ) ) in their skeletal muscles fail to express endogenously cleaved dystroglycan and have muscular dystrophy [ Neuromusc. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9897 | Dystrophic ProteinDG ( S654A ) muscles have reduced binding of antibodies, including VIA4 - 1, that recognize carbohydrate antigens on alpha dystroglycan, a finding similar to muscles in some forms of congenital muscular dystrophy. |
| 0.8732 | Dystrophic DG ( S654A ) muscles have reduced binding of antibodies, including VIA4 - 1, that recognize carbohydrate antigens on Proteinalpha dystroglycan , a finding similar to muscles in some forms of congenital muscular dystrophy. |
| 0.7869 | Dystrophic DG ( S654A ) muscles have reduced binding of antibodies, including VIA4 - 1, that recognize carbohydrate antigens on alpha Proteindystroglycan , a finding similar to muscles in some forms of congenital muscular dystrophy. |
| Score | Text |
|---|---|
| 0.9952 | Here we describe one ProteinDG ( S654A ) transgenic line where VIA4 - 1 antibody binding is absent in skeletal muscle. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.8865 | One such modification is likely to be the CT carbohydrate antigen, which is present on alpha dystroglycan in muscles overexpressing the ProteinCT GalNAc transferase [ Dev. |
| 0.5733 | One such modification is likely to be the CT carbohydrate antigen, which is present on alpha dystroglycan in muscles overexpressing the CT ProteinGalNAc transferase [ Dev. |
| 0.5548 | One such modification is likely to be the CT carbohydrate antigen, which is present on Proteinalpha dystroglycan in muscles overexpressing the CT GalNAc transferase [ Dev. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9634 | To test the relationship between the VIA4 - 1 and CT carbohydrate antigens, we made DG ( S654A ) / CT GalNAc transferase Protein( DG ( S654A ) / CT ) transgenic mice. |
| 0.9532 | To test the relationship between the VIA4 - 1 and CT carbohydrate antigens, we made ProteinDG ( S654A ) / CT GalNAc transferase ( DG ( S654A ) / CT ) transgenic mice. |
| 0.5933 | To test the relationship between the VIA4 - 1 and CT carbohydrate antigens, we made ProteinDG ( S654A ) / CT GalNAc transferase ( DG ( S654A ) / CT ) transgenic mice. |
| Score | Text |
|---|---|
| 0.9874 | Surprisingly, dystroglycan was cleaved, and alpha dystroglycan was glycosylated with the VIA4 - 1 antigen, in ProteinDG ( S654A ) / CT muscles. |
| 0.9872 | Surprisingly, Proteindystroglycan was cleaved, and alpha dystroglycan was glycosylated with the VIA4 - 1 antigen, in DG ( S654A ) / CT muscles. |
| 0.9840 | Surprisingly, dystroglycan was cleaved, and alpha dystroglycan was Glycosylationglycosylated with the VIA4 - 1 antigen, in DG ( S654A ) / CT muscles. |
| 0.7953 | Surprisingly, dystroglycan was cleaved, and Proteinalpha dystroglycan was glycosylated with the VIA4 - 1 antigen, in DG ( S654A ) / CT muscles. |
| 0.7708 | Surprisingly, dystroglycan was cleaved, and alpha Proteindystroglycan was glycosylated with the VIA4 - 1 antigen, in DG ( S654A ) / CT muscles. |
| Score | Text |
|---|---|
| 0.9986 | In addition, muscles in ProteinDG ( S654A ) / CT transgenic mice had little or no evidence of muscular dystrophy when compared to DG ( S654A ) littermates. |
| 0.9957 | In addition, muscles in DG ( S654A ) / CT transgenic mice had little or no evidence of muscular dystrophy when compared to ProteinDG ( S654A ) littermates. |
| Score | Text |
|---|---|
| 0.9948 | These experiments demonstrate that the CT GalNAc transferase can affect the post - translational processing of Proteindystroglycan and the extent of muscular dystrophy even in muscles where the VIA4 - 1 antigen is not present. |
| 0.9403 | These experiments demonstrate that the ProteinCT GalNAc transferase can affect the post - translational processing of dystroglycan and the extent of muscular dystrophy even in muscles where the VIA4 - 1 antigen is not present. |
| Score | Text |
|---|---|
| 0.9995 | Characterization of two novel proteins, NgRH1 and ProteinNgRH2 , structurally and biochemically homologous to the Nogo - 66 receptor. |
| 0.9993 | Characterization of two novel proteins, ProteinNgRH1 and NgRH2, structurally and biochemically homologous to the Nogo - 66 receptor. |
| 0.9235 | Characterization of two novel proteins, NgRH1 and NgRH2, structurally and biochemically homologous to the ProteinNogo - 66 receptor . |
| Score | Text |
|---|---|
| 0.9952 | Nogo - 66 receptor ( NgR ) has recently been identified as the neuronal receptor of the myelin - associated proteins ProteinNogo - A , oligodendrocyte protein ( OMgp ) and myelin - associated glycoprotein ( MAG ), and mediates inhibition of axonal regeneration both in vitro and in vivo. |
| 0.9863 | Nogo - 66 receptor Protein( NgR ) has recently been identified as the neuronal receptor of the myelin - associated proteins Nogo - A, oligodendrocyte protein ( OMgp ) and myelin - associated glycoprotein ( MAG ), and mediates inhibition of axonal regeneration both in vitro and in vivo. |
| 0.9735 | Nogo - 66 receptor ( NgR ) has recently been identified as the neuronal receptor of the myelin - associated proteins Nogo - A, oligodendrocyte protein Protein( OMgp ) and myelin - associated glycoprotein ( MAG ), and mediates inhibition of axonal regeneration both in vitro and in vivo. |
| 0.9712 | ProteinNogo - 66 receptor ( NgR ) has recently been identified as the neuronal receptor of the myelin - associated proteins Nogo - A, oligodendrocyte protein ( OMgp ) and myelin - associated glycoprotein ( MAG ), and mediates inhibition of axonal regeneration both in vitro and in vivo. |
| 0.9659 | Nogo - 66 receptor ( NgR ) has recently been identified as the neuronal receptor of the myelin - associated proteins Nogo - A, oligodendrocyte protein ( OMgp ) and myelin - associated glycoprotein Protein( MAG ) , and mediates inhibition of axonal regeneration both in vitro and in vivo. |
| 0.9487 | Nogo - 66 receptor ( NgR ) has recently been identified as the neuronal receptor of the myelin - associated proteins Nogo - A, Proteinoligodendrocyte protein ( OMgp ) and myelin - associated glycoprotein ( MAG ), and mediates inhibition of axonal regeneration both in vitro and in vivo. |
| 0.8808 | Nogo - 66 receptor ( NgR ) has recently been identified as the neuronal receptor of the myelin - associated proteins Nogo - A, oligodendrocyte protein ( OMgp ) and Proteinmyelin - associated glycoprotein ( MAG ), and mediates inhibition of axonal regeneration both in vitro and in vivo. |
| Score | Text |
|---|---|
| 0.9997 | Through database searches, we have identified two novel proteins ( NgRH1 and NgRH2 ) that turned out to be homologous in their primary structures, biochemical properties and expression patterns to ProteinNgR . |
| 0.9997 | Through database searches, we have identified two novel proteins ( NgRH1 and ProteinNgRH2 ) that turned out to be homologous in their primary structures, biochemical properties and expression patterns to NgR. |
| 0.9988 | Through database searches, we have identified two novel proteins Protein( NgRH1 and NgRH2 ) that turned out to be homologous in their primary structures, biochemical properties and expression patterns to NgR. |
| Score | Text |
|---|---|
| 0.9995 | Like ProteinNgR , the homologues contain eight leucine - rich repeats ( LRR ) flanked by a leucine - rich repeat C - terminus ( LRRCT ) and a leucine - rich repeat N - terminus ( LRRNT ), and also have a C - terminal GPI signal sequence. |
| Score | Text |
|---|---|
| 0.9997 | Northern blot analysis showed predominant expression of NgRH1 and ProteinNgRH2 mRNA in the brain. |
| 0.9996 | Northern blot analysis showed predominant expression of ProteinNgRH1 and NgRH2 mRNA in the brain. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9990 | NgRH1 and ProteinNgRH2 were detected on the cell surface of recombinant cell lines as N - glycosylated GPI anchored proteins and, consistent with other GPI anchored proteins, were localized within the lipid rafts of cellular membranes. |
| 0.9985 | ProteinNgRH1 and NgRH2 were detected on the cell surface of recombinant cell lines as N - glycosylated GPI anchored proteins and, consistent with other GPI anchored proteins, were localized within the lipid rafts of cellular membranes. |
| 0.9899 | NgRH1 and NgRH2 were detected on the cell surface of recombinant cell lines as GlycosylationN - glycosylated GPI anchored proteins and, consistent with other GPI anchored proteins, were localized within the lipid rafts of cellular membranes. |
| Score | Text |
|---|---|
| 0.9997 | In addition, an N - terminal proteolytic fragment of ProteinNgR comprising the majority of the ectodomain was found to be constitutively secreted from cells. |
| Score | Text |
|---|---|
| 0.9992 | Our data indicate that NgR, NgRH1 and ProteinNgRH2 constitute a novel receptor protein family, which may play related roles within the CNS. |
| 0.9986 | Our data indicate that NgR, ProteinNgRH1 and NgRH2 constitute a novel receptor protein family, which may play related roles within the CNS. |
| 0.9973 | Our data indicate that ProteinNgR , NgRH1 and NgRH2 constitute a novel receptor protein family, which may play related roles within the CNS. |
| Score | Text |
|---|---|
| 0.9438 | Synthesis of hydroxymethylglutathione from glutathione and L - serine catalyzed by Proteincarboxypeptidase Y . |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9779 | We found that carboxypeptidase Y Protein( CPY ) , but not carboxypeptidase A, catalyzed hmGSH synthesis from glutathione and L - serine in vitro at acidic pH. |
| 0.8863 | We found that Proteincarboxypeptidase Y ( CPY ), but not carboxypeptidase A, catalyzed hmGSH synthesis from glutathione and L - serine in vitro at acidic pH. |
| 0.8455 | We found that carboxypeptidase Y ( CPY ), but not Proteincarboxypeptidase A , catalyzed hmGSH synthesis from glutathione and L - serine in vitro at acidic pH. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9975 | Transcriptional elongation by RNA polymerase II and Proteinhistone methylation. |
| 0.9516 | Transcriptional elongation by RNA polymerase II and histone Methylationmethylation . |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9981 | In this article, we will review the recent literature linking the key biochemical process of transcriptional elongation by RNA polymerase II to histone methylation by COMPASS, ProteinDot1p , and Set2 methyltransferases. |
| 0.9981 | In this article, we will review the recent literature linking the key biochemical process of transcriptional elongation by RNA polymerase II to Proteinhistone methylation by COMPASS, Dot1p, and Set2 methyltransferases. |
| 0.9981 | In this article, we will review the recent literature linking the key biochemical process of transcriptional elongation by RNA polymerase II to histone methylation by COMPASS, Dot1p, and ProteinSet2 methyltransferases. |
| 0.5500 | In this article, we will review the recent literature linking the key biochemical process of transcriptional elongation by RNA polymerase II to histone Methylationmethylation by COMPASS, Dot1p, and Set2 methyltransferases. |
| In this article, we will review the recent literature linking the key biochemical process of transcriptional elongation by RNA polymerase II to histone Catalysismethylation by COMPASS, Dot1p, and Set2 methyltransferases. | |
| Score | Text |
|---|---|
| 0.9353 | Prolyl hydroxylation of collagen type I is required for efficient binding to integrin alpha 1 beta 1 and Proteinplatelet glycoprotein VI but not to alpha 2 beta 1. |
| 0.7942 | Prolyl hydroxylation of collagen type I is required for efficient binding to integrin alpha 1 beta 1 and platelet glycoprotein VI but not to alpha 2 Proteinbeta 1 . |
| 0.7669 | Prolyl hydroxylation of collagen type I is required for efficient binding to integrin alpha 1 beta 1 and platelet glycoprotein VI but not to Proteinalpha 2 beta 1. |
| 0.7274 | Prolyl hydroxylation of collagen type I is required for efficient binding to integrin alpha 1 Proteinbeta 1 and platelet glycoprotein VI but not to alpha 2 beta 1. |
| 0.7192 | Prolyl hydroxylation of collagen type I is required for efficient binding to Proteinintegrin alpha 1 beta 1 and platelet glycoprotein VI but not to alpha 2 beta 1. |
| 0.9459 | Prolyl hydroxylation of collagen type I is required for efficient binding to integrin alpha 1 beta 1 and platelet glycoprotein VI but not to Proteinalpha 2 beta 1 . |
| 0.9447 | Prolyl hydroxylation of collagen type I is required for efficient binding to Proteinintegrin alpha 1 beta 1 and platelet glycoprotein VI but not to alpha 2 beta 1. |
| 0.7023 | Prolyl hydroxylation of collagen type I is required for efficient binding to integrin alpha 1 beta 1 and platelet glycoprotein VI but not to Proteinalpha 2 beta 1. |
| 0.6902 | Prolyl hydroxylation of collagen type I is required for efficient binding to integrin alpha 1 beta 1 and platelet Proteinglycoprotein VI but not to alpha 2 beta 1. |
| 0.6827 | Prolyl hydroxylation of collagen type I is required for efficient binding to Proteinintegrin alpha 1 beta 1 and platelet glycoprotein VI but not to alpha 2 beta 1. |
| 0.6570 | Prolyl hydroxylation of collagen type I is required for efficient binding to integrin alpha 1 beta 1 and platelet glycoprotein VI but not to alpha Protein2 beta 1 . |
| 0.5569 | Prolyl hydroxylation of collagen type I is required for efficient binding to integrin alpha Protein1 beta 1 and platelet glycoprotein VI but not to alpha 2 beta 1. |
| 0.5300 | Prolyl hydroxylation of collagen type I is required for efficient binding to integrin Proteinalpha 1 beta 1 and platelet glycoprotein VI but not to alpha 2 beta 1. |
| Score | Text |
|---|---|
| 0.8100 | Collagen is a potent adhesive substrate for cells, an event essentially mediated by the integrins alpha 1 beta 1 and alpha 2 Proteinbeta 1 . |
| 0.6564 | Collagen is a potent adhesive substrate for cells, an event essentially mediated by the integrins alpha 1 beta 1 and Proteinalpha 2 beta 1. |
| 0.6361 | Collagen is a potent adhesive substrate for cells, an event essentially mediated by the Proteinintegrins alpha 1 beta 1 and alpha 2 beta 1. |
| 0.6072 | Collagen is a potent adhesive substrate for cells, an event essentially mediated by the integrins alpha 1 Proteinbeta 1 and alpha 2 beta 1. |
| 0.9314 | Collagen is a potent adhesive substrate for cells, an event essentially mediated by the integrins alpha 1 beta 1 and Proteinalpha 2 beta 1 . |
| 0.9018 | Collagen is a potent adhesive substrate for cells, an event essentially mediated by the Proteinintegrins alpha 1 beta 1 and alpha 2 beta 1. |
| 0.6696 | Collagen is a potent adhesive substrate for cells, an event essentially mediated by the integrins alpha 1 beta 1 and alpha Protein2 beta 1 . |
| 0.5961 | Collagen is a potent adhesive substrate for cells, an event essentially mediated by the Proteinintegrins alpha 1 beta 1 and alpha 2 beta 1. |
| 0.5501 | Collagen is a potent adhesive substrate for cells, an event essentially mediated by the integrins alpha 1 beta 1 and Proteinalpha 2 beta 1. |
| Score | Text |
|---|---|
| 0.8534 | Collagen fibrils also bind to the integrin alpha 2 beta 1 and the Proteinplatelet receptor glycoprotein VI to activate and aggregate platelets. |
| 0.8337 | Collagen fibrils also bind to the Proteinintegrin alpha 2 beta 1 and the platelet receptor glycoprotein VI to activate and aggregate platelets. |
| 0.7515 | Collagen fibrils also bind to the integrin alpha 2 Proteinbeta 1 and the platelet receptor glycoprotein VI to activate and aggregate platelets. |
| 0.9398 | Collagen fibrils also bind to the Proteinintegrin alpha 2 beta 1 and the platelet receptor glycoprotein VI to activate and aggregate platelets. |
| 0.8212 | Collagen fibrils also bind to the Proteinintegrin alpha 2 beta 1 and the platelet receptor glycoprotein VI to activate and aggregate platelets. |
| 0.6488 | Collagen fibrils also bind to the integrin alpha Protein2 beta 1 and the platelet receptor glycoprotein VI to activate and aggregate platelets. |
| 0.6096 | Collagen fibrils also bind to the integrin alpha 2 beta 1 and the platelet receptor Proteinglycoprotein VI to activate and aggregate platelets. |
| 0.5837 | Collagen fibrils also bind to the integrin alpha 2 beta 1 and the platelet Proteinreceptor glycoprotein VI to activate and aggregate platelets. |
| 0.5626 | Collagen fibrils also bind to the integrin Proteinalpha 2 beta 1 and the platelet receptor glycoprotein VI to activate and aggregate platelets. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.7679 | We show that alpha 2 Proteinbeta 1 but not alpha 1 beta 1 mediates cell adhesion to unhydroxylated collagen. |
| 0.7187 | We show that Proteinalpha 2 beta 1 but not alpha 1 beta 1 mediates cell adhesion to unhydroxylated collagen. |
| 0.6411 | We show that alpha 2 beta 1 but not alpha 1 Proteinbeta 1 mediates cell adhesion to unhydroxylated collagen. |
| 0.6122 | We show that alpha 2 beta 1 but not Proteinalpha 1 beta 1 mediates cell adhesion to unhydroxylated collagen. |
| 0.9010 | We show that Proteinalpha 2 beta 1 but not alpha 1 beta 1 mediates cell adhesion to unhydroxylated collagen. |
| 0.8705 | We show that alpha 2 beta 1 but not Proteinalpha 1 beta 1 mediates cell adhesion to unhydroxylated collagen. |
| 0.6512 | We show that alpha Protein2 beta 1 but not alpha 1 beta 1 mediates cell adhesion to unhydroxylated collagen. |
| 0.6263 | We show that Proteinalpha 2 beta 1 but not alpha 1 beta 1 mediates cell adhesion to unhydroxylated collagen. |
| Score | Text |
|---|---|
| 0.8606 | Soluble recombinant alpha 1 Proteinbeta 1 binding to unhydroxylated collagen is considerably reduced compared with bovine collagens, but binding can be restored by prolyl hydroxylation of recombinant collagen. |
| 0.7338 | Soluble recombinant Proteinalpha 1 beta 1 binding to unhydroxylated collagen is considerably reduced compared with bovine collagens, but binding can be restored by prolyl hydroxylation of recombinant collagen. |
| 0.8975 | Soluble recombinant Proteinalpha 1 beta 1 binding to unhydroxylated collagen is considerably reduced compared with bovine collagens, but binding can be restored by prolyl hydroxylation of recombinant collagen. |
| 0.8135 | Soluble recombinant alpha Protein1 beta 1 binding to unhydroxylated collagen is considerably reduced compared with bovine collagens, but binding can be restored by prolyl hydroxylation of recombinant collagen. |
| 0.6925 | Soluble recombinant Proteinalpha 1 beta 1 binding to unhydroxylated collagen is considerably reduced compared with bovine collagens, but binding can be restored by prolyl hydroxylation of recombinant collagen. |
| 0.5248 | Soluble recombinant alpha Protein1 beta 1 binding to unhydroxylated collagen is considerably reduced compared with bovine collagens, but binding can be restored by prolyl hydroxylation of recombinant collagen. |
| Score | Text |
|---|---|
| 0.9418 | We also show that platelets use alpha 2 Proteinbeta 1 to adhere to the unhydroxylated recombinant molecules, but the adhesion is weaker than on fully hydroxylated collagen, and the unhydroxylated collagen fibrils fail to aggregate platelets. |
| 0.8463 | We also show that platelets use Proteinalpha 2 beta 1 to adhere to the unhydroxylated recombinant molecules, but the adhesion is weaker than on fully hydroxylated collagen, and the unhydroxylated collagen fibrils fail to aggregate platelets. |
| 0.9671 | We also show that platelets use Proteinalpha 2 beta 1 to adhere to the unhydroxylated recombinant molecules, but the adhesion is weaker than on fully hydroxylated collagen, and the unhydroxylated collagen fibrils fail to aggregate platelets. |
| 0.9109 | We also show that platelets use alpha Protein2 beta 1 to adhere to the unhydroxylated recombinant molecules, but the adhesion is weaker than on fully hydroxylated collagen, and the unhydroxylated collagen fibrils fail to aggregate platelets. |
| 0.8095 | We also show that platelets use Proteinalpha 2 beta 1 to adhere to the unhydroxylated recombinant molecules, but the adhesion is weaker than on fully hydroxylated collagen, and the unhydroxylated collagen fibrils fail to aggregate platelets. |
| 0.6020 | We also show that platelets use alpha Protein2 beta 1 to adhere to the unhydroxylated recombinant molecules, but the adhesion is weaker than on fully hydroxylated collagen, and the unhydroxylated collagen fibrils fail to aggregate platelets. |
| Score | Text |
|---|---|
| 0.9091 | Prolyl hydroxylation is thus required for binding of collagen to Proteinplatelet glycoprotein VI and to cells by alpha 1 beta 1. |
| 0.8324 | Prolyl hydroxylation is thus required for binding of collagen to platelet glycoprotein VI and to cells by alpha 1 Proteinbeta 1 . |
| 0.6804 | Prolyl hydroxylation is thus required for binding of collagen to platelet glycoprotein VI and to cells by Proteinalpha 1 beta 1. |
| 0.9264 | Prolyl hydroxylation is thus required for binding of collagen to platelet glycoprotein VI and to cells by Proteinalpha 1 beta 1 . |
| 0.7171 | Prolyl hydroxylation is thus required for binding of collagen to platelet glycoprotein VI and to cells by alpha Protein1 beta 1 . |
| 0.6073 | Prolyl hydroxylation is thus required for binding of collagen to platelet glycoprotein VI and to cells by Proteinalpha 1 beta 1. |
| 0.5952 | Prolyl hydroxylation is thus required for binding of collagen to platelet Proteinglycoprotein VI and to cells by alpha 1 beta 1. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9920 | Mechanism, mutagenesis, and chemical rescue of a Proteinbeta - mannosidase from cellulomonas fimi. |
| Score | Text |
|---|---|
| 0.9940 | The chemical mechanism of a retaining Proteinbeta - mannosidase from Cellulomonas fimi has been characterized through steady - state kinetic analyses with a range of substrates, coupled with chemical rescue studies on both the wild - type enzyme and mutants in which active site carboxyl groups have been replaced. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9971 | The tentative assignment of E429 as the acid - base catalyst of ProteinMan2A on the basis of sequence alignments with other family 2 glycosidases was confirmed by the increased turnover rate observed for the mutant E429A in the presence of azide and fluoride, leading to the production of beta - mannosyl azide and beta - mannosyl fluoride, respectively. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9968 | Substantial oxocarbenium ion character at the transition state was demonstrated by the alpha - deuterium kinetic isotope effect for ProteinMan2A E429A of alpha - D ( V ) = 1. 12 + / - 0. 01. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9856 | Likely involvement of acid / base catalysis was revealed by the pH dependence of k ( cat ) for ProteinMan2A E429A, which follows a bell - shaped profile described by pK ( a ) values of 6. 1 and 8. 4, substantially different from that of the wild - type enzyme. |
| Score | Text |
|---|---|
| 0.9930 | The glycosidic bond cleaving activity of ProteinMan2A E519A and E519S nucleophile mutants is restored with azide and fluoride and appears to correlate with the corresponding " glycosynthase " activities. |
| Score | Text |
|---|---|
| 0.9983 | The contribution of the substrate 2 - hydroxyl to stabilization of the ProteinMan2A glycosylation transition state ( DeltaDeltaG ( ) = 5. 1 kcal mol ( - 1 ) ) was probed using a 2 - deoxymannose substrate. |
| Score | Text |
|---|---|
| 0.7864 | This value, surprisingly, is comparable to that found from equivalent studies with Proteinbeta - glucosidases despite the geometric differences at C - 2 and the importance of hydrogen bonding at that position. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9896 | Occurrence of O - linked Xyl - GlcNAc and EntityXyl - Glc disaccharides in trocarin, a factor Xa homolog from snake venom. |
| 0.9890 | Occurrence of O - linked EntityXyl - GlcNAc and Xyl - Glc disaccharides in trocarin, a factor Xa homolog from snake venom. |
| 0.9839 | Occurrence of O - linked Xyl - GlcNAc and Xyl - Glc disaccharides in Proteintrocarin , a factor Xa homolog from snake venom. |
| 0.9321 | Occurrence of O - linked Xyl - GlcNAc and Xyl - Glc disaccharides in trocarin, a Proteinfactor Xa homolog from snake venom. |
| 0.7677 | Occurrence of GlycosylationO - linked Xyl - GlcNAc and Xyl - Glc disaccharides in trocarin, a factor Xa homolog from snake venom. |
| Score | Text |
|---|---|
| 0.9992 | ProteinTrocarin is a 46515 - Da group D prothrombin - activating glycoprotein from the venom of the Australian elapid, Tropidechis carinatus. |
| 0.9932 | Trocarin is a 46515 - Da group D Proteinprothrombin - activating glycoprotein from the venom of the Australian elapid, Tropidechis carinatus. |
| Score | Text |
|---|---|
| 0.9985 | Amino acid sequencing and functional characterization of Proteintrocarin demonstrated that it is a structural and functional homolog of mammalian blood coagulation factor ( F ) Xa. |
| 0.6913 | Amino acid sequencing and functional characterization of trocarin demonstrated that it is a structural and functional homolog of mammalian blood Proteincoagulation factor ( F ) Xa . |
| Score | Text |
|---|---|
| 0.9912 | In this study we show that, in contrast to mammalian Xa, which is not Glycosylationglycosylated , trocarin contains an O - linked carbohydrate moiety in its light chain and an N - linked carbohydrate oligosaccharide in its heavy chain. |
| 0.9650 | In this study we show that, in contrast to mammalian Xa, which is not glycosylated, Proteintrocarin contains an O - linked carbohydrate moiety in its light chain and an N - linked carbohydrate oligosaccharide in its heavy chain. |
| 0.9144 | In this study we show that, in contrast to mammalian Xa, which is not glycosylated, trocarin contains an GlycosylationO - linked carbohydrate moiety in its light chain and an N - linked carbohydrate oligosaccharide in its heavy chain. |
| 0.8990 | In this study we show that, in contrast to mammalian Xa, which is not glycosylated, trocarin contains an O - linked carbohydrate moiety in its light chain and an GlycosylationN - linked carbohydrate oligosaccharide in its heavy chain. |
| 0.8868 | In this study we show that, in contrast to mammalian ProteinXa , which is not glycosylated, trocarin contains an O - linked carbohydrate moiety in its light chain and an N - linked carbohydrate oligosaccharide in its heavy chain. |
| 0.7687 | In this study we show that, in contrast to mammalian Xa, which is not glycosylated, trocarin contains an O - linked carbohydrate moiety in its light chain and an N - linked carbohydrate oligosaccharide in its Entityheavy chain . |
| 0.7522 | In this study we show that, in contrast to mammalian Xa, which is not glycosylated, trocarin contains an O - linked carbohydrate moiety in its light chain and an N - linked Entitycarbohydrate oligosaccharide in its heavy chain. |
| 0.6818 | In this study we show that, in contrast to mammalian Xa, which is not glycosylated, trocarin contains an O - linked carbohydrate moiety in its Entitylight chain and an N - linked carbohydrate oligosaccharide in its heavy chain. |
| 0.6305 | In this study we show that, in contrast to mammalian Xa, which is not glycosylated, trocarin contains an O - linked Entitycarbohydrate moiety in its light chain and an N - linked carbohydrate oligosaccharide in its heavy chain. |
| 0.8622 | In this study we show that, in contrast to mammalian Xa, which is not glycosylated, trocarin contains an O - linked carbohydrate moiety in its light chain and an N - linked carbohydrate Entityoligosaccharide in its heavy chain. |
| 0.8159 | In this study we show that, in contrast to mammalian Xa, which is not glycosylated, trocarin contains an O - linked carbohydrate moiety in its light Entitychain and an N - linked carbohydrate oligosaccharide in its heavy chain. |
| 0.8087 | In this study we show that, in contrast to mammalian Xa, which is not glycosylated, trocarin contains an O - linked carbohydrate moiety in its light chain and an N - linked carbohydrate oligosaccharide in its heavy Entitychain . |
| 0.7069 | In this study we show that, in contrast to mammalian Xa, which is not glycosylated, trocarin contains an O - linked carbohydrate moiety in its light chain and an N - linked carbohydrate oligosaccharide in its Entityheavy chain. |
| 0.6974 | In this study we show that, in contrast to mammalian Xa, which is not glycosylated, trocarin contains an O - linked carbohydrate Entitymoiety in its light chain and an N - linked carbohydrate oligosaccharide in its heavy chain. |
| 0.6749 | In this study we show that, in contrast to mammalian Xa, which is not glycosylated, trocarin contains an O - linked carbohydrate moiety in its light chain and an N - linked Entitycarbohydrate oligosaccharide in its heavy chain. |
| 0.5696 | In this study we show that, in contrast to mammalian Xa, which is not glycosylated, trocarin contains an O - linked Entitycarbohydrate moiety in its light chain and an N - linked carbohydrate oligosaccharide in its heavy chain. |
| 0.5134 | In this study we show that, in contrast to mammalian Xa, which is not glycosylated, trocarin contains an O - linked carbohydrate moiety in its Entitylight chain and an N - linked carbohydrate oligosaccharide in its heavy chain. |
| Score | Text |
|---|---|
| 0.9855 | Mass spectrometry and sugar compositional analysis indicate that the O - linked carbohydrate moiety is a mixture of Xyl - GlcNAc -, EntityGlcNAc - , Xyl - Glc - and Glc - structures linked to Ser 52. |
| 0.9813 | Mass spectrometry and sugar compositional analysis indicate that the O - linked carbohydrate moiety is a mixture of Xyl - GlcNAc -, GlcNAc -, EntityXyl - Glc - and Glc - structures linked to Ser 52. |
| 0.9705 | Mass spectrometry and sugar compositional analysis indicate that the O - linked carbohydrate moiety is a mixture of EntityXyl - GlcNAc - , GlcNAc -, Xyl - Glc - and Glc - structures linked to Ser 52. |
| 0.9619 | Mass spectrometry and sugar compositional analysis indicate that the O - linked carbohydrate moiety is a mixture of Xyl - GlcNAc -, GlcNAc -, Xyl - Glc - and EntityGlc - structures linked to Ser 52. |
| 0.9477 | Mass spectrometry and sugar compositional analysis indicate that the GlycosylationO - linked carbohydrate moiety is a mixture of Xyl - GlcNAc -, GlcNAc -, Xyl - Glc - and Glc - structures linked to Ser 52. |
| 0.8243 | Mass spectrometry and sugar compositional analysis indicate that the O - linked carbohydrate moiety is a mixture of Xyl - GlcNAc -, GlcNAc -, Xyl - Glc - and Glc - structures linked to EntitySer 52 . |
| 0.7969 | Mass spectrometry and sugar compositional analysis indicate that the O - linked carbohydrate moiety is a mixture of Xyl - GlcNAc -, GlcNAc -, Xyl - Glc - and EntityGlc - structures linked to Ser 52. |
| Score | Text |
|---|---|
| 0.9811 | The N - linked carbohydrate on Asn 45 of the heavy chain is a sialylated, diantennary oligosaccharide that is located at the lip of the active site of the Proteinprothrombin activator. |
| 0.9423 | The GlycosylationN - linked carbohydrate on Asn 45 of the heavy chain is a sialylated, diantennary oligosaccharide that is located at the lip of the active site of the prothrombin activator. |
| 0.9020 | The N - linked carbohydrate on EntityAsn 45 of the heavy chain is a sialylated, diantennary oligosaccharide that is located at the lip of the active site of the prothrombin activator. |
| 0.7438 | The N - linked Entitycarbohydrate on Asn 45 of the heavy chain is a sialylated, diantennary oligosaccharide that is located at the lip of the active site of the prothrombin activator. |
| 0.5997 | The N - linked carbohydrate on Asn 45 of the heavy chain is a sialylated, diantennary Entityoligosaccharide that is located at the lip of the active site of the prothrombin activator. |
| 0.5575 | The N - linked carbohydrate on EntityAsn 45 of the heavy chain is a sialylated, diantennary oligosaccharide that is located at the lip of the active site of the prothrombin activator. |
| The N - linked carbohydrate on Asn 45 of the heavy chain is a Entitysialylated, diantennary oligosaccharide that is located at the lip of the active site of the prothrombin activator. | |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9825 | The low density lipoprotein ( LDL ) receptor - related protein 1 Protein( LRP1 ) belongs to a growing number of cell surface proteins that undergo regulated proteolytic processing that culminates in the release of their intracellular domain ( ICD ) by the intramembranous protease gamma - secretase. |
| 0.5787 | The Proteinlow density lipoprotein ( LDL ) receptor - related protein 1 ( LRP1 ) belongs to a growing number of cell surface proteins that undergo regulated proteolytic processing that culminates in the release of their intracellular domain ( ICD ) by the intramembranous protease gamma - secretase. |
| Score | Text |
|---|---|
| 0.9970 | Here we show that ProteinLRP1 is differentially glycosylated in a tissue - specific manner and that carbohydrate addition reduces proteolytic cleavage of the extracellular domain and, concomitantly, ICD release. |
| 0.9955 | Here we show that LRP1 is differentially Glycosylationglycosylated in a tissue - specific manner and that carbohydrate addition reduces proteolytic cleavage of the extracellular domain and, concomitantly, ICD release. |
| Score | Text |
|---|---|
| 0.9797 | The apolipoprotein E ( apoE ) receptor - 2 Protein( apoER2 ) , another member of the LDL receptor family with functions in cellular signal transmission, also undergoes sequential proteolytic processing, resulting in intracellular domain release into the cytoplasm. |
| The Proteinapolipoprotein E ( apoE ) receptor - 2 ( apoER2 ), another member of the LDL receptor family with functions in cellular signal transmission, also undergoes sequential proteolytic processing, resulting in intracellular domain release into the cytoplasm. | |
| Score | Text |
|---|---|
| 0.9980 | The penultimate processing step also involves cleavage of the ProteinapoER2 extracellular domain. |
| Score | Text |
|---|---|
| 0.9695 | The rate at which this cleavage step occurs is determined by the Glycosylationglycosylation state of the receptor, which in turn is regulated by the alternative splicing of an exon encoding several O - linked sugar attachment sites. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9998 | Inactivation of Proteinp16 gene in leukemia. |
| Score | Text |
|---|---|
| 0.9998 | To determine the frequency of Proteinp16 gene inactivation in leukemia cells, and to evaluate their value in the prediction of their clinical outcome. |
| Score | Text |
|---|---|
| 0.9990 | Bone marrow or peripheral blood samples from 48 patients with leukemia were examined by multiplex polymerase chain reaction ( MPCR ) to detect p16 gene homozygous deletion, and restriction enzyme PCR to detect Proteinp16 gene methylation. p16 gene inactivation were detected in 10 of the 48 patients ( 20. 4 % ). |
| 0.9989 | Bone marrow or peripheral blood samples from 48 patients with leukemia were examined by multiplex polymerase chain reaction ( MPCR ) to detect Proteinp16 gene homozygous deletion, and restriction enzyme PCR to detect p16 gene methylation. p16 gene inactivation were detected in 10 of the 48 patients ( 20. 4 % ). |
| 0.9989 | Bone marrow or peripheral blood samples from 48 patients with leukemia were examined by multiplex polymerase chain reaction ( MPCR ) to detect p16 gene homozygous deletion, and restriction enzyme PCR to detect p16 gene methylation. Proteinp16 gene inactivation were detected in 10 of the 48 patients ( 20. 4 % ). |
| 0.9972 | Bone marrow or peripheral blood samples from 48 patients with leukemia were examined by multiplex polymerase chain reaction ( MPCR ) to detect p16 gene homozygous deletion, and restriction enzyme PCR to detect p16 gene DNA_methylationmethylation . p16 gene inactivation were detected in 10 of the 48 patients ( 20. 4 % ). |
| Score | Text |
|---|---|
| 0.9993 | They were five patients with Proteinp16 homozygous deletion, and five patients with p16 methylation, respectively. p16 gene inactivation correlates with adverse prognosis features. |
| 0.9981 | They were five patients with p16 homozygous deletion, and five patients with p16 methylation, respectively. Proteinp16 gene inactivation correlates with adverse prognosis features. |
| 0.9966 | They were five patients with p16 homozygous deletion, and five patients with Proteinp16 methylation, respectively. p16 gene inactivation correlates with adverse prognosis features. |
| 0.9877 | They were five patients with p16 homozygous deletion, and five patients with p16 DNA_methylationmethylation , respectively. p16 gene inactivation correlates with adverse prognosis features. |
| Score | Text |
|---|---|
| 0.9998 | The patients with p16 inactivation had poor response to chemotherapy, and had significantly shorter survival times than the patients in whom Proteinp16 gene was preserved ( P < 0. 001 ). |
| 0.9998 | The patients with Proteinp16 inactivation had poor response to chemotherapy, and had significantly shorter survival times than the patients in whom p16 gene was preserved ( P < 0. 001 ). |
| Score | Text |
|---|---|
| 0.9999 | The inactivation of Proteinp16 gene play a key role in the pathogenesis and the progression of some leukemia. |
| Score | Text |
|---|---|
| 0.9998 | The detection of Proteinp16 gene is reliable prognostic factor that predict shortened survival times. |
| Score | Text |
|---|---|
| 0.9955 | A haploid affair : core Proteinhistone transitions during spermatogenesis. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9968 | Therefore, an analysis of the role of Proteinhistone variants and modifications in these processes may shed light upon the mechanisms involved and the control of chromatin structure in general. |
| Score | Text |
|---|---|
| 0.9946 | Histone variants such as histone H3. 3, ProteinH2AX , and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), ubiquitination of histones H2A and H2B ( uH2A, uH2B ), and phosphorylation of histone H3 ( H3p ). |
| 0.9895 | Histone variants such as histone H3. 3, H2AX, and ProteinmacroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), ubiquitination of histones H2A and H2B ( uH2A, uH2B ), and phosphorylation of histone H3 ( H3p ). |
| 0.9845 | Histone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), ubiquitination of Proteinhistones H2A and H2B ( uH2A, uH2B ), and phosphorylation of histone H3 ( H3p ). |
| 0.9843 | ProteinHistone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), ubiquitination of histones H2A and H2B ( uH2A, uH2B ), and phosphorylation of histone H3 ( H3p ). |
| 0.9743 | Histone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), ubiquitination of histones H2A and H2B ( uH2A, ProteinuH2B ) , and phosphorylation of histone H3 ( H3p ). |
| 0.9689 | Histone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of Proteinhistone H4 ( acH4 ), ubiquitination of histones H2A and H2B ( uH2A, uH2B ), and phosphorylation of histone H3 ( H3p ). |
| 0.9676 | Histone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), ubiquitination of histones H2A and ProteinH2B ( uH2A, uH2B ), and phosphorylation of histone H3 ( H3p ). |
| 0.9651 | Histone variants such as Proteinhistone H3. 3 , H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), ubiquitination of histones H2A and H2B ( uH2A, uH2B ), and phosphorylation of histone H3 ( H3p ). |
| 0.9373 | Histone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), Ubiquitinationubiquitination of histones H2A and H2B ( uH2A, uH2B ), and phosphorylation of histone H3 ( H3p ). |
| 0.9341 | Histone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), ubiquitination of histones H2A and H2B Protein( uH2A , uH2B ), and phosphorylation of histone H3 ( H3p ). |
| 0.9341 | Histone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), ubiquitination of histones H2A and H2B ( uH2A, uH2B ), and Phosphorylationphosphorylation of histone H3 ( H3p ). |
| 0.9327 | Histone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 Protein( acH4 ) , ubiquitination of histones H2A and H2B ( uH2A, uH2B ), and phosphorylation of histone H3 ( H3p ). |
| 0.9241 | Histone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), ubiquitination of histones H2A and H2B ( uH2A, uH2B ), and phosphorylation of histone H3 Protein( H3p ) . |
| 0.9062 | Histone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), ubiquitination of histones H2A and H2B ( uH2A, uH2B ), and phosphorylation of Proteinhistone H3 ( H3p ). |
| 0.8937 | Histone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated Acetylationacetylation of histone H4 ( acH4 ), ubiquitination of histones H2A and H2B ( uH2A, uH2B ), and phosphorylation of histone H3 ( H3p ). |
| 0.9158 | Histone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), ubiquitination of histones H2A and ProteinH2B ( uH2A , uH2B ), and phosphorylation of histone H3 ( H3p ). |
| 0.9029 | Histone variants such as Proteinhistone H3 . 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), ubiquitination of histones H2A and H2B ( uH2A, uH2B ), and phosphorylation of histone H3 ( H3p ). |
| 0.7177 | Histone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), ubiquitination of Proteinhistones H2A and H2B ( uH2A, uH2B ), and phosphorylation of histone H3 ( H3p ). |
| 0.6610 | Histone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), ubiquitination of histones ProteinH2A and H2B ( uH2A, uH2B ), and phosphorylation of histone H3 ( H3p ). |
| 0.6304 | Histone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of Proteinhistone H4 ( acH4 ) , ubiquitination of histones H2A and H2B ( uH2A, uH2B ), and phosphorylation of histone H3 ( H3p ). |
| Score | Text |
|---|---|
| 0.9976 | This review will examine recent discoveries concerning the role of Proteinhistone modifications and variants during meiosis and spermatogenesis. |
| Score | Text |
|---|---|
| 0.9982 | HIF prolyl - hydroxylase 2 is the key oxygen sensor setting low steady - state levels of ProteinHIF - 1alpha in normoxia. |
| 0.8177 | ProteinHIF prolyl - hydroxylase 2 is the key oxygen sensor setting low steady - state levels of HIF - 1alpha in normoxia. |
| Score | Text |
|---|---|
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| 0.9855 | In normoxia, the HIF - alpha subunits are targeted for destruction by prolyl hydroxylation, a specific modification that provides recognition for the E3 Proteinubiquitin ligase complex containing the von Hippel - Lindau tumour suppressor protein ( pVHL ). |
| 0.9764 | In normoxia, the HIF - alpha subunits are targeted for destruction by prolyl hydroxylation, a specific modification that provides recognition for the E3 ubiquitin ligase complex containing the von Hippel - Lindau tumour suppressor protein Protein( pVHL ) . |
| 0.8452 | In normoxia, the HIF - alpha subunits are targeted for destruction by prolyl hydroxylation, a specific modification that provides recognition for the E3 ubiquitin ligase complex containing the Proteinvon Hippel - Lindau tumour suppressor protein ( pVHL ). |
| 0.7291 | In normoxia, the HIF - alpha subunits are targeted for destruction by prolyl hydroxylation, a specific modification that provides recognition for the E3 ubiquitin ligase complex containing the von ProteinHippel - Lindau tumour suppressor protein ( pVHL ). |
| 0.6931 | In normoxia, the HIF - alpha subunits are targeted for destruction by prolyl hydroxylation, a specific modification that provides recognition for the E3 ubiquitin ligase complex containing the von Hippel - Lindau Proteintumour suppressor protein ( pVHL ). |
| Score | Text |
|---|---|
| 0.9990 | Three HIF prolyl - hydroxylases ( PHD1, Protein2 and 3 ) were identified recently in mammals and shown to hydroxylate HIF - alpha subunits. |
| 0.9976 | Three HIF prolyl - hydroxylases ( PHD1, 2 and Protein3 ) were identified recently in mammals and shown to hydroxylate HIF - alpha subunits. |
| 0.9942 | Three HIF prolyl - hydroxylases Protein( PHD1 , 2 and 3 ) were identified recently in mammals and shown to hydroxylate HIF - alpha subunits. |
| Score | Text |
|---|---|
| 0.9998 | Here we show that specific'silencing'of ProteinPHD2 with short interfering RNAs is sufficient to stabilize and activate HIF - 1alpha in normoxia in all the human cells investigated.'Silencing'of PHD1 and PHD3 has no effect on the stability of HIF - 1alpha either in normoxia or upon re - oxygenation of cells briefly exposed to hypoxia. |
| 0.9998 | Here we show that specific'silencing'of PHD2 with short interfering RNAs is sufficient to stabilize and activate HIF - 1alpha in normoxia in all the human cells investigated.'Silencing'of PHD1 and ProteinPHD3 has no effect on the stability of HIF - 1alpha either in normoxia or upon re - oxygenation of cells briefly exposed to hypoxia. |
| 0.9998 | Here we show that specific'silencing'of PHD2 with short interfering RNAs is sufficient to stabilize and activate HIF - 1alpha in normoxia in all the human cells investigated.'Silencing'of ProteinPHD1 and PHD3 has no effect on the stability of HIF - 1alpha either in normoxia or upon re - oxygenation of cells briefly exposed to hypoxia. |
| 0.9995 | Here we show that specific'silencing'of PHD2 with short interfering RNAs is sufficient to stabilize and activate HIF - 1alpha in normoxia in all the human cells investigated.'Silencing'of PHD1 and PHD3 has no effect on the stability of ProteinHIF - 1alpha either in normoxia or upon re - oxygenation of cells briefly exposed to hypoxia. |
| 0.9994 | Here we show that specific'silencing'of PHD2 with short interfering RNAs is sufficient to stabilize and activate ProteinHIF - 1alpha in normoxia in all the human cells investigated.'Silencing'of PHD1 and PHD3 has no effect on the stability of HIF - 1alpha either in normoxia or upon re - oxygenation of cells briefly exposed to hypoxia. |
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|---|---|
| 0.9997 | We therefore conclude that, in vivo, PHDs have distinct assigned functions, ProteinPHD2 being the critical oxygen sensor setting the low steady - state levels of HIF - 1alpha in normoxia. |
| 0.9993 | We therefore conclude that, in vivo, PHDs have distinct assigned functions, PHD2 being the critical oxygen sensor setting the low steady - state levels of ProteinHIF - 1alpha in normoxia. |
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|---|---|
| 0.9997 | Interestingly, ProteinPHD2 is upregulated by hypoxia, providing an HIF - 1 - dependent auto - regulatory mechanism driven by the oxygen tension. |
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|---|---|
| 0.9993 | Insulation of the chicken beta - globin chromosomal domain from a chromatin - condensing protein, ProteinMENT . |
| 0.9720 | Insulation of the chicken Proteinbeta - globin chromosomal domain from a chromatin - condensing protein, MENT. |
| Score | Text |
|---|---|
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| 0.9994 | We mapped the topography of a terminal stage - specific chromatin - condensing protein, ProteinMENT , across the active chicken beta - globin domain. |
| 0.9894 | We mapped the topography of a terminal stage - specific chromatin - condensing protein, MENT, across the active chicken Proteinbeta - globin domain. |
| Score | Text |
|---|---|
| 0.9990 | We observed two sharp transitions of ProteinMENT concentration coinciding with the beta - globin boundary elements. |
| 0.9971 | We observed two sharp transitions of MENT concentration coinciding with the Proteinbeta - globin boundary elements. |
| Score | Text |
|---|---|
| 0.9977 | The ProteinMENT distribution profile was opposite to that of acetylated core histones but correlated with that of histone H3 dimethylated at lysine 9 ( H3me2K9 ). |
| 0.9802 | The MENT distribution profile was opposite to that of acetylated core Proteinhistones but correlated with that of histone H3 dimethylated at lysine 9 ( H3me2K9 ). |
| 0.9703 | The MENT distribution profile was opposite to that of Acetylationacetylated core histones but correlated with that of histone H3 dimethylated at lysine 9 ( H3me2K9 ). |
| 0.9696 | The MENT distribution profile was opposite to that of acetylated core histones but correlated with that of histone H3 Methylationdimethylated at lysine 9 ( H3me2K9 ). |
| 0.9544 | The MENT distribution profile was opposite to that of acetylated core histones but correlated with that of Proteinhistone H3 dimethylated at lysine 9 ( H3me2K9 ). |
| 0.8819 | The MENT distribution profile was opposite to that of acetylated core histones but correlated with that of histone H3 dimethylated at Entitylysine 9 ( H3me2K9 ). |
| 0.5393 | The MENT distribution profile was opposite to that of acetylated core histones but correlated with that of histone H3 dimethylated at lysine 9 Entity( H3me2K9 ) . |
| The MENT distribution profile was opposite to that of acetylated core histones but correlated with that of histone H3 dimethylated at lysine 9 Protein( H3me2K9 ) . | |
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|---|---|
| 0.9986 | Ectopic ProteinMENT expression in NIH 3T3 cells caused a large - scale and specific remodeling of chromatin marked by H3me2K9. |
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| 0.9990 | ProteinMENT colocalized with H3me2K9 both in chicken erythrocytes and NIH 3T3 cells. |
| 0.9532 | MENT colocalized with ProteinH3me2K9 both in chicken erythrocytes and NIH 3T3 cells. |
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|---|---|
| 0.9991 | Mutational analysis of ProteinMENT and experiments with deacetylase inhibitors revealed the essential role of the reaction center loop domain and an inhibitory affect of histone hyperacetylation on the MENT - induced chromatin remodeling in vivo. |
| 0.9899 | Mutational analysis of MENT and experiments with deacetylase inhibitors revealed the essential role of the reaction center loop domain and an inhibitory affect of histone hyperacetylation on the ProteinMENT - induced chromatin remodeling in vivo. |
| 0.9848 | Mutational analysis of MENT and experiments with deacetylase inhibitors revealed the essential role of the reaction center loop domain and an inhibitory affect of Proteinhistone hyperacetylation on the MENT - induced chromatin remodeling in vivo. |
| 0.9657 | Mutational analysis of MENT and experiments with deacetylase inhibitors revealed the essential role of the reaction center loop domain and an inhibitory affect of histone Acetylationhyperacetylation on the MENT - induced chromatin remodeling in vivo. |
| Score | Text |
|---|---|
| 0.9971 | In vitro, the elimination of the histone H3 N - terminal peptide containing lysine 9 by trypsin blocked chromatin self - association by ProteinMENT , while reconstitution with dimethylated but not acetylated N - terminal domain of histone H3 specifically restored chromatin self - association by MENT. |
| 0.9966 | In vitro, the elimination of the histone H3 N - terminal peptide containing lysine 9 by trypsin blocked chromatin self - association by MENT, while reconstitution with dimethylated but not acetylated N - terminal domain of histone H3 specifically restored chromatin self - association by ProteinMENT . |
| 0.9753 | In vitro, the elimination of the histone H3 N - terminal peptide containing lysine 9 by trypsin blocked chromatin self - association by MENT, while reconstitution with dimethylated but not acetylated N - terminal domain of Proteinhistone H3 specifically restored chromatin self - association by MENT. |
| 0.9649 | In vitro, the elimination of the Proteinhistone H3 N - terminal peptide containing lysine 9 by trypsin blocked chromatin self - association by MENT, while reconstitution with dimethylated but not acetylated N - terminal domain of histone H3 specifically restored chromatin self - association by MENT. |
| 0.9461 | In vitro, the elimination of the histone H3 N - terminal peptide containing lysine 9 by trypsin blocked chromatin self - association by MENT, while reconstitution with Methylationdimethylated but not acetylated N - terminal domain of histone H3 specifically restored chromatin self - association by MENT. |
| 0.9369 | In vitro, the elimination of the histone H3 N - terminal peptide containing lysine 9 by trypsin blocked chromatin self - association by MENT, while reconstitution with dimethylated but not Acetylationacetylated N - terminal domain of histone H3 specifically restored chromatin self - association by MENT. |
| 0.7865 | In vitro, the elimination of the histone H3 N - terminal peptide containing lysine 9 by trypsin blocked chromatin self - association by MENT, while reconstitution with dimethylated but not acetylated EntityN - terminal domain of histone H3 specifically restored chromatin self - association by MENT. |
| 0.6977 | In vitro, the elimination of the histone H3 N - terminal peptide containing lysine 9 by trypsin blocked chromatin self - association by MENT, while reconstitution with dimethylated but not acetylated EntityN - terminal domain of histone H3 specifically restored chromatin self - association by MENT. |
| 0.6568 | In vitro, the elimination of the histone H3 N - terminal peptide containing Entitylysine 9 by trypsin blocked chromatin self - association by MENT, while reconstitution with dimethylated but not acetylated N - terminal domain of histone H3 specifically restored chromatin self - association by MENT. |
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|---|---|
| 0.9996 | We suggest that histone H3 modification at lysine 9 directly regulates chromatin condensation by recruiting ProteinMENT to chromatin in a fashion that is spatially constrained from active genes by gene boundary elements and histone hyperacetylation. |
| 0.9942 | We suggest that histone H3 modification at lysine 9 directly regulates chromatin condensation by recruiting MENT to chromatin in a fashion that is spatially constrained from active genes by gene boundary elements and Proteinhistone hyperacetylation. |
| 0.9781 | We suggest that Proteinhistone H3 modification at lysine 9 directly regulates chromatin condensation by recruiting MENT to chromatin in a fashion that is spatially constrained from active genes by gene boundary elements and histone hyperacetylation. |
| 0.9725 | We suggest that histone H3 modification at lysine 9 directly regulates chromatin condensation by recruiting MENT to chromatin in a fashion that is spatially constrained from active genes by gene boundary elements and histone Acetylationhyperacetylation . |
| 0.5107 | We suggest that histone H3 modification at Entitylysine 9 directly regulates chromatin condensation by recruiting MENT to chromatin in a fashion that is spatially constrained from active genes by gene boundary elements and histone hyperacetylation. |
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|---|---|
| 0.9996 | Requirement for Proteinneo1p in retrograde transport from the Golgi complex to the endoplasmic reticulum. |
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|---|---|
| 0.9993 | ProteinNeo1p from Saccharomyces cerevisiae is an essential P - type ATPase and potential aminophospholipid translocase ( flippase ) in the Drs2p family. |
| 0.9971 | Neo1p from Saccharomyces cerevisiae is an essential P - type ATPase and potential aminophospholipid translocase ( flippase ) in the ProteinDrs2p family. |
| Score | Text |
|---|---|
| 0.9997 | We have previously implicated ProteinDrs2p in protein transport steps in the late secretory pathway requiring ADP - ribosylation factor ( ARF ) and clathrin. |
| Score | Text |
|---|---|
| 0.9995 | Here, we present evidence that epitope - tagged ProteinNeo1p localizes to the endoplasmic reticulum ( ER ) and Golgi complex and is required for a retrograde transport pathway between these organelles. |
| Score | Text |
|---|---|
| 0.9998 | Using conditional alleles of ProteinNEO1 , we find that loss of Neo1p function causes cargo - specific defects in anterograde protein transport early in the secretory pathway and perturbs glycosylation in the Golgi complex. |
| 0.9996 | Using conditional alleles of NEO1, we find that loss of ProteinNeo1p function causes cargo - specific defects in anterograde protein transport early in the secretory pathway and perturbs glycosylation in the Golgi complex. |
| Score | Text |
|---|---|
| 0.9997 | ProteinRer1 - GFP , a protein that cycles between the ER and Golgi complex in COPI and COPII vesicles, is mislocalized to the vacuole in neo1 - ts at the nonpermissive temperature. |
| 0.9994 | Rer1 - GFP, a protein that cycles between the ER and Golgi complex in COPI and COPII vesicles, is mislocalized to the vacuole in Proteinneo1 - ts at the nonpermissive temperature. |
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| 0.9852 | Recombinant ProteinL - ferritin showed less precipitation even above a pH of 8. 65. |
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| 0.9962 | ProteinHistone hyperacetylation in mitosis prevents sister chromatid separation and produces chromosome segregation defects. |
| 0.9733 | Histone Acetylationhyperacetylation in mitosis prevents sister chromatid separation and produces chromosome segregation defects. |
| Score | Text |
|---|---|
| 0.9936 | Posttranslational modifications of core Proteinhistones contribute to driving changes in chromatin conformation and compaction. |
| Score | Text |
|---|---|
| 0.9982 | Herein, we investigated the role of histone deacetylation on the mitotic process by inhibiting Proteinhistone deacetylases shortly before mitosis in human primary fibroblasts. |
| 0.9976 | Herein, we investigated the role of Proteinhistone deacetylation on the mitotic process by inhibiting histone deacetylases shortly before mitosis in human primary fibroblasts. |
| 0.8260 | Herein, we investigated the role of histone Deacetylationdeacetylation on the mitotic process by inhibiting histone deacetylases shortly before mitosis in human primary fibroblasts. |
| Score | Text |
|---|---|
| 0.9981 | Cells entering mitosis with hyperacetylated Proteinhistones displayed altered chromatin conformation associated with decreased reactivity to the anti - Ser 10 phospho H3 antibody, increased recruitment of protein phosphatase 1 - delta on mitotic chromosomes, and depletion of heterochromatin protein 1 from the centromeric heterochromatin. |
| 0.9821 | Cells entering mitosis with Acetylationhyperacetylated histones displayed altered chromatin conformation associated with decreased reactivity to the anti - Ser 10 phospho H3 antibody, increased recruitment of protein phosphatase 1 - delta on mitotic chromosomes, and depletion of heterochromatin protein 1 from the centromeric heterochromatin. |
| 0.9808 | Cells entering mitosis with hyperacetylated histones displayed altered chromatin conformation associated with decreased reactivity to the anti - Ser 10 phospho ProteinH3 antibody, increased recruitment of protein phosphatase 1 - delta on mitotic chromosomes, and depletion of heterochromatin protein 1 from the centromeric heterochromatin. |
| Cells entering mitosis with hyperacetylated histones displayed altered chromatin conformation associated with decreased reactivity to the anti - Ser 10 phospho H3 antibody, increased recruitment of Proteinprotein phosphatase 1 - delta on mitotic chromosomes, and depletion of heterochromatin protein 1 from the centromeric heterochromatin. | |
| Score | Text |
|---|---|
| 0.9980 | Inhibition of Proteinhistone deacetylation before mitosis produced defective chromosome condensation and impaired mitotic progression in living cells, suggesting that improper chromosome condensation may induce mitotic checkpoint activation. |
| 0.8839 | Inhibition of histone Deacetylationdeacetylation before mitosis produced defective chromosome condensation and impaired mitotic progression in living cells, suggesting that improper chromosome condensation may induce mitotic checkpoint activation. |
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| 0.9959 | Lagging chromosomes consisting of single or paired sisters were also induced by the presence of hyperacetylated Proteinhistones , indicating that the less constrained centromeric organization associated with heterochromatin protein 1 depletion may promote the attachment of kinetochores to microtubules coming from both poles. |
| 0.9890 | Lagging chromosomes consisting of single or paired sisters were also induced by the presence of Acetylationhyperacetylated histones, indicating that the less constrained centromeric organization associated with heterochromatin protein 1 depletion may promote the attachment of kinetochores to microtubules coming from both poles. |
| Score | Text |
|---|---|
| 0.9939 | Hydroxylated kininogens and Proteinkinins . |
| 0.9793 | Hydroxylated Proteinkininogens and kinins. |
| 0.8546 | HydroxylationHydroxylated kininogens and kinins. |
| Score | Text |
|---|---|
| 0.9824 | ProteinHydroxyprolyl - 3 - bradykinin was identified in the digest of purified human high molecular weight ( H ) kininogen with plasma kallikrein. |
| 0.9182 | Hydroxyprolyl - 3 - bradykinin was identified in the digest of purified human high molecular weight ( H ) kininogen with Proteinplasma kallikrein . |
| 0.9063 | Hydroxyprolyl - 3 - bradykinin was identified in the digest of purified human high molecular weight ( H ) kininogen with plasma Proteinkallikrein . |
| Hydroxyprolyl - 3 - bradykinin was identified in the digest of purified human Proteinhigh molecular weight ( H ) kininogen with plasma kallikrein. | |
| Score | Text |
|---|---|
| 0.9069 | Hydroxyproline was not detected in the heavy and light chains portions of ProteinH kininogen , although they include three possible sites for hydroxylation of proline by proline hydroxylase. |
| 0.7060 | Hydroxyproline was not detected in the heavy and light chains portions of H kininogen, although they include three possible sites for Hydroxylationhydroxylation of proline by proline hydroxylase. |
| 0.5596 | Hydroxyproline was not detected in the heavy and light chains portions of H Proteinkininogen , although they include three possible sites for hydroxylation of proline by proline hydroxylase. |
| Score | Text |
|---|---|
| 0.9973 | The content of hydroxyprolyl - 3 - bradykinin in H kininogen from individual plasmas varied from 14 % to 64 % of total Proteinkinin . |
| 0.9842 | The content of Proteinhydroxyprolyl - 3 - bradykinin in H kininogen from individual plasmas varied from 14 % to 64 % of total kinin. |
| 0.8891 | The content of hydroxyprolyl - 3 - bradykinin in ProteinH kininogen from individual plasmas varied from 14 % to 64 % of total kinin. |
| 0.5702 | The content of hydroxyprolyl - 3 - bradykinin in H Proteinkininogen from individual plasmas varied from 14 % to 64 % of total kinin. |
| Score | Text |
|---|---|
| 0.9690 | The present results and our previous results indicate that only Proteinkinin moity in H kininogen from human and monkey plasmas has been partially hydroxylated post - translationally by proline - 4 - hydroxylase. |
| 0.8933 | The present results and our previous results indicate that only kinin moity in ProteinH kininogen from human and monkey plasmas has been partially hydroxylated post - translationally by proline - 4 - hydroxylase. |
| 0.6976 | The present results and our previous results indicate that only kinin moity in H kininogen from human and monkey plasmas has been partially Hydroxylationhydroxylated post - translationally by proline - 4 - hydroxylase. |
| 0.6174 | The present results and our previous results indicate that only kinin moity in H kininogen from human and monkey plasmas has been partially hydroxylated post - translationally by Proteinproline - 4 - hydroxylase . |
| 0.5876 | The present results and our previous results indicate that only kinin moity in H Proteinkininogen from human and monkey plasmas has been partially hydroxylated post - translationally by proline - 4 - hydroxylase. |
| 0.5086 | The present results and our previous results indicate that only kinin moity in ProteinH kininogen from human and monkey plasmas has been partially hydroxylated post - translationally by proline - 4 - hydroxylase. |
| Score | Text |
|---|---|
| 0.9407 | Purification and characterization of soluble forms of human and rat Proteinstem cell factor recombinantly expressed by Escherichia coli and by Chinese hamster ovary cells. |
| Score | Text |
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| 0.9647 | Stem cell factor Protein( SCF ) is a novel, early - acting hematopoietic factor. |
| 0.6746 | ProteinStem cell factor ( SCF ) is a novel, early - acting hematopoietic factor. |
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| 0.9998 | We have recombinantly expressed forms of human and rat ProteinSCF corresponding to the soluble, processed form in Escherichia coli and in Chinese hamster ovary ( CHO ) cells. |
| Score | Text |
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| 0.9970 | After expression in E. coli, folding and oxidation of the ProteinSCF polypeptides are required. |
| Score | Text |
|---|---|
| 0.9934 | The ProteinSCFs expressed in CHO cells are secreted into the medium in active state and, like the natural SCF, are glycosylated. |
| 0.9844 | The SCFs expressed in CHO cells are secreted into the medium in active state and, like the natural ProteinSCF , are glycosylated. |
| 0.9834 | The SCFs expressed in CHO cells are secreted into the medium in active state and, like the natural SCF, are Glycosylationglycosylated . |
| Score | Text |
|---|---|
| 0.9993 | Purification of the recombinant ProteinSCFs is described. |
| Score | Text |
|---|---|
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| 0.9809 | Inhibition of fusion by neutralizing monoclonal antibodies to the Proteinhaemagglutinin - neuraminidase glycoprotein of Newcastle disease virus. |
| Score | Text |
|---|---|
| 0.9728 | The majority of neutralizing monoclonal antibodies ( MAbs ) to the Proteinhaemagglutinin - neuraminidase ( HN ) glycoprotein of Newcastle disease virus prevent attachment of the virus to cellular receptors and inhibits virion - induced fusion from without ( FFWO ) and fusion from within ( FFWI ) mediated by the virus glycoprotein - laden infected cell surface. |
| 0.9529 | The majority of neutralizing monoclonal antibodies ( MAbs ) to the haemagglutinin - neuraminidase Protein( HN ) glycoprotein of Newcastle disease virus prevent attachment of the virus to cellular receptors and inhibits virion - induced fusion from without ( FFWO ) and fusion from within ( FFWI ) mediated by the virus glycoprotein - laden infected cell surface. |
| Score | Text |
|---|---|
| 0.9948 | For these antibodies, the inhibition of fusion is presumed to be the result of the prevention of ProteinHN - mediated bridging of potential fusion partners. |
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| 0.9972 | This suggests that the requirement for ProteinHN may be different in the two modes of fusion. |
| Score | Text |
|---|---|
| 0.9983 | The epitopes recognized by MAbs to sites 3 and 4 have been delineated by the identification of individual nucleotide substitutions in the ProteinHN genes of neutralization escape variants. |
| Score | Text |
|---|---|
| 0.9536 | Some of the deduced amino acid substitutions result in additional N - linked glycosylation sites in ProteinHN , which are utilized and presumably account for the escape from neutralization. |
| 0.8201 | Some of the deduced amino acid substitutions result in additional EntityN - linked glycosylation sites in HN, which are utilized and presumably account for the escape from neutralization. |
| 0.8191 | Some of the deduced amino acid substitutions result in additional N - linked glycosylation sites in HN, which are Glycosylationutilized and presumably account for the escape from neutralization. |
| 0.8283 | Some of the deduced amino acid substitutions result in additional N - linked Entityglycosylation sites in HN, which are utilized and presumably account for the escape from neutralization. |
| 0.7204 | Some of the deduced amino acid substitutions result in additional N - linked Entityglycosylation sites in HN, which are utilized and presumably account for the escape from neutralization. |
| 0.6617 | Some of the deduced amino acid substitutions result in additional EntityN - linked glycosylation sites in HN, which are utilized and presumably account for the escape from neutralization. |
| 0.4769 | Some of the deduced amino acid substitutions result in additional EntityN - linked glycosylation sites in HN, which are utilized and presumably account for the escape from neutralization. |
| Score | Text |
|---|---|
| 0.9976 | The influence of N - linked glycosylation on the antigenicity and immunogenicity of rubella virus ProteinE1 glycoprotein. |
| 0.8220 | The influence of GlycosylationN - linked glycosylation on the antigenicity and immunogenicity of rubella virus E1 glycoprotein. |
| 0.8842 | The influence of N - linked Glycosylationglycosylation on the antigenicity and immunogenicity of rubella virus E1 glycoprotein. |
| Score | Text |
|---|---|
| 0.9992 | Rubella virus ProteinE1 glycoprotein contains three functional N - linked glycosylation sites. |
| Score | Text |
|---|---|
| 0.9989 | The role of N - linked glycosylation on the antigenicity and immunogenicity of ProteinE1 glycoprotein was studied using vaccinia recombinants expressing E1 glycosylation mutants. |
| 0.9953 | The role of N - linked glycosylation on the antigenicity and immunogenicity of E1 glycoprotein was studied using vaccinia recombinants expressing ProteinE1 glycosylation mutants. |
| 0.8824 | The role of GlycosylationN - linked glycosylation on the antigenicity and immunogenicity of E1 glycoprotein was studied using vaccinia recombinants expressing E1 glycosylation mutants. |
| 0.8918 | The role of N - linked Glycosylationglycosylation on the antigenicity and immunogenicity of E1 glycoprotein was studied using vaccinia recombinants expressing E1 glycosylation mutants. |
| 0.7445 | The role of GlycosylationN - linked glycosylation on the antigenicity and immunogenicity of E1 glycoprotein was studied using vaccinia recombinants expressing E1 glycosylation mutants. |
| Score | Text |
|---|---|
| 0.9990 | Expressed E1 glycosylation mutant proteins were recognized by a panel of E1 - specific monoclonal antibodies in radioimmunoprecipitation, immunofluorescence, and immunoblotting, indicating that carbohydrate side chains on ProteinE1 are not involved in the constitution of epitopes recognized by these monoclonal antibodies. |
| 0.9989 | Expressed E1 glycosylation mutant proteins were recognized by a panel of ProteinE1 - specific monoclonal antibodies in radioimmunoprecipitation, immunofluorescence, and immunoblotting, indicating that carbohydrate side chains on E1 are not involved in the constitution of epitopes recognized by these monoclonal antibodies. |
| 0.9976 | Expressed ProteinE1 glycosylation mutant proteins were recognized by a panel of E1 - specific monoclonal antibodies in radioimmunoprecipitation, immunofluorescence, and immunoblotting, indicating that carbohydrate side chains on E1 are not involved in the constitution of epitopes recognized by these monoclonal antibodies. |
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|---|---|
| 0.9987 | This observation was further supported by the fact that removal of oligosaccharides on E1 by glycosidase digestion did not significantly change the antigenicity of ProteinE1 . |
| 0.9968 | This observation was further supported by the fact that removal of oligosaccharides on ProteinE1 by glycosidase digestion did not significantly change the antigenicity of E1. |
| Score | Text |
|---|---|
| 0.9974 | All the glycosylation mutants were capable of eliciting anti - RV ProteinE1 antibodies. |
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| 0.9982 | Our findings suggest that although carbohydrate on E1 is not directly involved in the antigenic structures of ProteinE1 , it is important in maintaining proper protein folding and stable conformation for expression of immunological epitopes on E1. |
| 0.9982 | Our findings suggest that although carbohydrate on ProteinE1 is not directly involved in the antigenic structures of E1, it is important in maintaining proper protein folding and stable conformation for expression of immunological epitopes on E1. |
| 0.9979 | Our findings suggest that although carbohydrate on E1 is not directly involved in the antigenic structures of E1, it is important in maintaining proper protein folding and stable conformation for expression of immunological epitopes on ProteinE1 . |
| Score | Text |
|---|---|
| 0.9534 | GlycosylationGlycosylation of the interleukin - 1 receptor type I is required for optimal binding of interleukin - 1. |
| 0.8109 | Glycosylation of the Proteininterleukin - 1 receptor type I is required for optimal binding of interleukin - 1. |
| Score | Text |
|---|---|
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| 0.9895 | To determine the role of Glycosylationglycosylation of the IL - 1 receptor type I ( IL - 1RtI ) in the binding and function of IL - 1, we used four plant lectins and glycosidase treatment on two different T - cell lines ( EL4 - 6. 1 and D10S ) and expressing high number of binding sites for IL - 1. |
| 0.9695 | To determine the role of glycosylation of the IL - 1 receptor type I Protein( IL - 1RtI ) in the binding and function of IL - 1, we used four plant lectins and glycosidase treatment on two different T - cell lines ( EL4 - 6. 1 and D10S ) and expressing high number of binding sites for IL - 1. |
| 0.9090 | To determine the role of glycosylation of the ProteinIL - 1 receptor type I ( IL - 1RtI ) in the binding and function of IL - 1, we used four plant lectins and glycosidase treatment on two different T - cell lines ( EL4 - 6. 1 and D10S ) and expressing high number of binding sites for IL - 1. |
| 0.8954 | To determine the role of glycosylation of the IL - 1 receptor type I ( IL - 1RtI ) in the binding and function of IL - 1, we used four plant lectins and glycosidase treatment on two different T - cell lines ( EL4 - 6. 1 and D10S ) and expressing high number of binding sites for ProteinIL - 1 . |
| 0.6039 | To determine the role of glycosylation of the IL - 1 receptor type I ( IL - 1RtI ) in the binding and function of ProteinIL - 1 , we used four plant lectins and glycosidase treatment on two different T - cell lines ( EL4 - 6. 1 and D10S ) and expressing high number of binding sites for IL - 1. |
| Score | Text |
|---|---|
| 0.9197 | The lectins wheat germ agglutinin, phytohemagglutinin, and Proteinconcanavalin A inhibited in a dose - response manner the IL - 1 - induced proliferation of D10S cells. |
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|---|---|
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|---|---|
| 0.9902 | Digestion by N - glycosidase significantly decreased the capacity of cells to bind IL - 1, and reduced by approximately 20, 000 D the M ( r ) of the ProteinIL - 1RtI . |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9839 | This study demonstrates that Glycosylationglycosylation of the extracellular domain of the IL - 1RtI is due to N - linked carbohydrates, that the degree of glycosylation can vary in cells of different lineage, and that this N - linked glycosylation appears to be essential for optimal binding and activity of IL - 1 to its type I receptor. |
| 0.9773 | This study demonstrates that glycosylation of the extracellular domain of the IL - 1RtI is due to N - linked carbohydrates, that the degree of Glycosylationglycosylation can vary in cells of different lineage, and that this N - linked glycosylation appears to be essential for optimal binding and activity of IL - 1 to its type I receptor. |
| 0.9554 | This study demonstrates that glycosylation of the extracellular domain of the IL - 1RtI is due to N - linked carbohydrates, that the degree of glycosylation can vary in cells of different lineage, and that this GlycosylationN - linked glycosylation appears to be essential for optimal binding and activity of IL - 1 to its type I receptor. |
| 0.9376 | This study demonstrates that glycosylation of the extracellular domain of the IL - 1RtI is due to N - linked Entitycarbohydrates , that the degree of glycosylation can vary in cells of different lineage, and that this N - linked glycosylation appears to be essential for optimal binding and activity of IL - 1 to its type I receptor. |
| 0.7725 | This study demonstrates that glycosylation of the extracellular domain of the ProteinIL - 1RtI is due to N - linked carbohydrates, that the degree of glycosylation can vary in cells of different lineage, and that this N - linked glycosylation appears to be essential for optimal binding and activity of IL - 1 to its type I receptor. |
| 0.9880 | This study demonstrates that glycosylation of the extracellular domain of the IL - 1RtI is due to N - linked carbohydrates, that the degree of glycosylation can vary in cells of different lineage, and that this N - linked glycosylation appears to be essential for optimal binding and activity of ProteinIL - 1 to its type I receptor. |
| 0.9640 | This study demonstrates that glycosylation of the extracellular domain of the IL - 1RtI is due to N - linked carbohydrates, that the degree of glycosylation can vary in cells of different lineage, and that this N - linked Glycosylationglycosylation appears to be essential for optimal binding and activity of IL - 1 to its type I receptor. |
| 0.8293 | This study demonstrates that glycosylation of the extracellular domain of the IL - 1RtI is due to N - linked carbohydrates, that the degree of glycosylation can vary in cells of different lineage, and that this GlycosylationN - linked glycosylation appears to be essential for optimal binding and activity of IL - 1 to its type I receptor. |
| 0.4637 | This study demonstrates that glycosylation of the extracellular domain of the IL - 1RtI is due to GlycosylationN - linked carbohydrates, that the degree of glycosylation can vary in cells of different lineage, and that this N - linked glycosylation appears to be essential for optimal binding and activity of IL - 1 to its type I receptor. |
| Score | Text |
|---|---|
| 0.9991 | Expression of ProteinCpgp40 / 15 in Toxoplasma gondii : a surrogate system for the study of Cryptosporidium glycoprotein antigens. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9997 | The glycoprotein products of the Cpgp40 / 15 gene, gp40 and Proteingp15 , are involved in C. parvum sporozoite attachment to and invasion of host cells and, as such, may be good targets for anticryptosporidial therapies. |
| 0.9996 | The glycoprotein products of the Cpgp40 / 15 gene, Proteingp40 and gp15, are involved in C. parvum sporozoite attachment to and invasion of host cells and, as such, may be good targets for anticryptosporidial therapies. |
| 0.9990 | The glycoprotein products of the ProteinCpgp40 / 15 gene, gp40 and gp15, are involved in C. parvum sporozoite attachment to and invasion of host cells and, as such, may be good targets for anticryptosporidial therapies. |
| Score | Text |
|---|---|
| 0.9575 | However, the function of these antigens appears to be dependent on the presence of multiple O - linked Entityalpha - N - acetylgalactosamine ( alpha - GalNAc ) determinants. |
| 0.9502 | However, the function of these antigens appears to be dependent on the presence of multiple GlycosylationO - linked alpha - N - acetylgalactosamine ( alpha - GalNAc ) determinants. |
| 0.9233 | However, the function of these antigens appears to be dependent on the presence of multiple O - linked alpha - N - acetylgalactosamine Entity( alpha - GalNAc ) determinants. |
| 0.6846 | However, the function of these antigens appears to be dependent on the presence of multiple O - linked Entityalpha - N - acetylgalactosamine ( alpha - GalNAc ) determinants. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9989 | As a unique approach to this problem, the ProteinCpgp40 / 15 gene was transiently expressed in Toxoplasma gondii, and the expressed recombinant glycoproteins were characterized. |
| Score | Text |
|---|---|
| 0.9998 | Antisera to gp40 and Proteingp15 reacted with the surface membranes of tachyzoites expressing the Cpgp40 / 15 construct, and this reactivity colocalized with that of antiserum to the T. gondii surface protein SAG1. |
| 0.9996 | Antisera to gp40 and gp15 reacted with the surface membranes of tachyzoites expressing the ProteinCpgp40 / 15 construct, and this reactivity colocalized with that of antiserum to the T. gondii surface protein SAG1. |
| 0.9996 | Antisera to Proteingp40 and gp15 reacted with the surface membranes of tachyzoites expressing the Cpgp40 / 15 construct, and this reactivity colocalized with that of antiserum to the T. gondii surface protein SAG1. |
| 0.9995 | Antisera to gp40 and gp15 reacted with the surface membranes of tachyzoites expressing the Cpgp40 / 15 construct, and this reactivity colocalized with that of antiserum to the T. gondii surface protein ProteinSAG1 . |
| Score | Text |
|---|---|
| 0.9981 | Surface membrane localization was dependent on the presence of the glycophosphatidylinositol anchor attachment site present in the Proteingp15 coding sequence. |
| Score | Text |
|---|---|
| 0.9955 | The presence of terminal O - linked alpha - GalNAc determinants on the T. gondii recombinant Proteingp40 was confirmed by reactivity with Helix pomatia lectin and the monoclonal antibody 4E9, which recognizes alpha - GalNAc residues, and digestion with alpha - N - acetylgalactosaminidase. |
| 0.9929 | The presence of terminal O - linked Entityalpha - GalNAc determinants on the T. gondii recombinant gp40 was confirmed by reactivity with Helix pomatia lectin and the monoclonal antibody 4E9, which recognizes alpha - GalNAc residues, and digestion with alpha - N - acetylgalactosaminidase. |
| 0.9624 | The presence of terminal GlycosylationO - linked alpha - GalNAc determinants on the T. gondii recombinant gp40 was confirmed by reactivity with Helix pomatia lectin and the monoclonal antibody 4E9, which recognizes alpha - GalNAc residues, and digestion with alpha - N - acetylgalactosaminidase. |
| 0.9794 | The presence of terminal O - linked alpha - GalNAc determinants on the T. gondii recombinant gp40 was confirmed by reactivity with Helix pomatia lectin and the monoclonal antibody 4E9, which recognizes alpha - GalNAc residues, and digestion with Proteinalpha - N - acetylgalactosaminidase . |
| 0.7244 | The presence of terminal O - linked alpha - GalNAc determinants on the T. gondii recombinant gp40 was confirmed by reactivity with Helix pomatia lectin and the monoclonal antibody 4E9, which recognizes Entityalpha - GalNAc residues, and digestion with alpha - N - acetylgalactosaminidase. |
| 0.5534 | The presence of terminal O - linked alpha - GalNAc determinants on the T. gondii recombinant gp40 was confirmed by reactivity with Helix pomatia lectin and the monoclonal antibody 4E9, which recognizes Entityalpha - GalNAc residues , and digestion with alpha - N - acetylgalactosaminidase. |
| Score | Text |
|---|---|
| 0.9995 | In addition to appropriate localization and glycosylation, T. gondii apparently processes the gp40 / 15 precursor into the gp40 and Proteingp15 component glycopolypeptides, albeit inefficiently. |
| 0.9990 | In addition to appropriate localization and glycosylation, T. gondii apparently processes the gp40 / 15 precursor into the Proteingp40 and gp15 component glycopolypeptides, albeit inefficiently. |
| 0.9982 | In addition to appropriate localization and glycosylation, T. gondii apparently processes the Proteingp40 / 15 precursor into the gp40 and gp15 component glycopolypeptides, albeit inefficiently. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9962 | Aberrant methylation of ProteinDAP - kinase in therapy - related acute myeloid leukemia and myelodysplastic syndromes. |
| 0.9670 | Aberrant DNA_methylationmethylation of DAP - kinase in therapy - related acute myeloid leukemia and myelodysplastic syndromes. |
| Score | Text |
|---|---|
| 0.9698 | Death - associated protein kinase Protein( DAP - kinase ) , a proapoptotic serine / threonine kinase, is a candidate tumor suppressor gene. |
| 0.8802 | ProteinDeath - associated protein kinase ( DAP - kinase ), a proapoptotic serine / threonine kinase, is a candidate tumor suppressor gene. |
| Score | Text |
|---|---|
| 0.9948 | We studied the methylation status of ProteinDAP - kinase of 194 bone marrow samples from 160 patients with acute myeloid leukemia ( AML ) and 34 with a myelodysplastic syndrome ( MDS ) at the time of initial diagnosis by polymerase chain reaction ( PCR ). |
| 0.9888 | We studied the DNA_methylationmethylation status of DAP - kinase of 194 bone marrow samples from 160 patients with acute myeloid leukemia ( AML ) and 34 with a myelodysplastic syndrome ( MDS ) at the time of initial diagnosis by polymerase chain reaction ( PCR ). |
| Score | Text |
|---|---|
| 0.9984 | Hypermethylation of ProteinDAP - kinase was present in 27. 5 % ( 44 of 160 ) of AML and in 47 % ( 16 of 34 ) of MDS specimens and significantly correlated to loss of DAP - kinase expression ( P =. 008 ). |
| 0.9769 | DNA_methylationHypermethylation of DAP - kinase was present in 27. 5 % ( 44 of 160 ) of AML and in 47 % ( 16 of 34 ) of MDS specimens and significantly correlated to loss of DAP - kinase expression ( P =. 008 ). |
| 0.8817 | Hypermethylation of DAP - kinase was present in 27. 5 % ( 44 of 160 ) of AML and in 47 % ( 16 of 34 ) of MDS specimens and significantly correlated to loss of ProteinDAP - kinase expression ( P =. 008 ). |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9871 | ProteinDAP - kinase hypermethylation in AML was associated with myelodysplastic changes in the bone marrow at the time of the initial diagnosis ( P =. 002 ) and with the presence of cytogenetic abnormalities ( P =. 02 ). |
| 0.9825 | DAP - kinase DNA_methylationhypermethylation in AML was associated with myelodysplastic changes in the bone marrow at the time of the initial diagnosis ( P =. 002 ) and with the presence of cytogenetic abnormalities ( P =. 02 ). |
| Score | Text |
|---|---|
| 0.9987 | Alteration in the apoptotic response due to the loss of ProteinDAP - kinase function may be an early event in the transformation pathway to secondary leukemia via myelodysplasia. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9979 | DNA from paraffin - embedded tissue of 6 APAs was evaluated for microsatellite instability ( MI ), MLH - 1 promoter hypermethylation, and ProteinCTNNB - 1 mutations. |
| 0.9890 | DNA from paraffin - embedded tissue of 6 APAs was evaluated for microsatellite instability ( MI ), MLH - 1 Entitypromoter hypermethylation, and CTNNB - 1 mutations. |
| 0.9818 | DNA from paraffin - embedded tissue of 6 APAs was evaluated for microsatellite instability ( MI ), MLH - 1 promoter DNA_methylationhypermethylation , and CTNNB - 1 mutations. |
| 0.9682 | DNA from paraffin - embedded tissue of 6 APAs was evaluated for microsatellite instability ( MI ), ProteinMLH - 1 promoter hypermethylation, and CTNNB - 1 mutations. |
| Score | Text |
|---|---|
| 0.9992 | Tissue sections were also subjected to MLH - 1, ProteinMSH - 2 , and beta - catenin immunostaining. |
| 0.9981 | Tissue sections were also subjected to MLH - 1, MSH - 2, and Proteinbeta - catenin immunostaining. |
| 0.9925 | Tissue sections were also subjected to ProteinMLH - 1 , MSH - 2, and beta - catenin immunostaining. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9870 | Two tumors exhibited ProteinMLH - 1 promoter hypermethylation and showed focal negative MHL - 1 immunostaining ; 1 of these showed marked architectural complexity and cellular pleomorphism. |
| 0.9864 | Two tumors exhibited MLH - 1 promoter DNA_methylationhypermethylation and showed focal negative MHL - 1 immunostaining ; 1 of these showed marked architectural complexity and cellular pleomorphism. |
| 0.9824 | Two tumors exhibited MLH - 1 Entitypromoter hypermethylation and showed focal negative MHL - 1 immunostaining ; 1 of these showed marked architectural complexity and cellular pleomorphism. |
| Score | Text |
|---|---|
| 0.9996 | Five cases presented Proteinbeta - catenin nuclear immunoreactivity, but none of them had CTNNB - 1 mutations. |
| 0.9971 | Five cases presented beta - catenin nuclear immunoreactivity, but none of them had ProteinCTNNB - 1 mutations. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9910 | Some APAs exhibit MLH - 1 promoter DNA_methylationhypermethylation with focal lack of MLH - 1 immunostaining, a molecular abnormality involved in the transition from complex atypical hyperplasia to endometrioid adenocarcinoma. |
| 0.9863 | Some APAs exhibit ProteinMLH - 1 promoter hypermethylation with focal lack of MLH - 1 immunostaining, a molecular abnormality involved in the transition from complex atypical hyperplasia to endometrioid adenocarcinoma. |
| 0.9695 | Some APAs exhibit MLH - 1 Entitypromoter hypermethylation with focal lack of MLH - 1 immunostaining, a molecular abnormality involved in the transition from complex atypical hyperplasia to endometrioid adenocarcinoma. |
| 0.8882 | Some APAs exhibit MLH - 1 promoter hypermethylation with focal lack of ProteinMLH - 1 immunostaining, a molecular abnormality involved in the transition from complex atypical hyperplasia to endometrioid adenocarcinoma. |
| Score | Text |
|---|---|
| 0.9941 | A common polymorphism in the oxygen - dependent degradation ( ODD ) domain of hypoxia inducible factor - 1alpha ( HIF - 1alpha ) does not impair EntityPro - 564 hydroxylation. |
| 0.9544 | A common polymorphism in the oxygen - dependent degradation ( ODD ) domain of hypoxia inducible factor - 1alpha ( HIF - 1alpha ) does not impair Pro - 564 Hydroxylationhydroxylation . |
| 0.9011 | A common polymorphism in the oxygen - dependent degradation ( ODD ) domain of hypoxia inducible factor - 1alpha Protein( HIF - 1alpha ) does not impair Pro - 564 hydroxylation. |
| 0.8000 | A common polymorphism in the oxygen - dependent degradation ( ODD ) domain of Proteinhypoxia inducible factor - 1alpha ( HIF - 1alpha ) does not impair Pro - 564 hydroxylation. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9968 | Under normoxic conditions, the alpha subunit of HIF is rapidly degraded in a manner dependent on hydroxylation of two conserved proline residues at positions 402 and 564 in ProteinHIF - 1alpha in the oxygen - dependent degradation ( ODD ) domain. |
| 0.9745 | Under normoxic conditions, the alpha subunit of HIF is rapidly degraded in a manner dependent on Hydroxylationhydroxylation of two conserved proline residues at positions 402 and 564 in HIF - 1alpha in the oxygen - dependent degradation ( ODD ) domain. |
| 0.8789 | Under normoxic conditions, the alpha subunit of HIF is rapidly degraded in a manner dependent on hydroxylation of two conserved Entityproline residues at positions 402 and 564 in HIF - 1alpha in the oxygen - dependent degradation ( ODD ) domain. |
| 0.6517 | Under normoxic conditions, the alpha subunit of HIF is rapidly degraded in a manner dependent on hydroxylation of two conserved Entityproline residues at positions 402 and 564 in HIF - 1alpha in the oxygen - dependent degradation ( ODD ) domain. |
| Score | Text |
|---|---|
| 0.9993 | This allows subsequent recognition by the von Hippel - Lindau ( VHL ) tumor suppressor protein, which targets HIF for degradation by the Proteinubiquitin - proteasome pathway. |
| 0.8779 | This allows subsequent recognition by the von Hippel - Lindau Protein( VHL ) tumor suppressor protein, which targets HIF for degradation by the ubiquitin - proteasome pathway. |
| This allows subsequent recognition by the Proteinvon Hippel - Lindau ( VHL ) tumor suppressor protein, which targets HIF for degradation by the ubiquitin - proteasome pathway. | |
| Score | Text |
|---|---|
| 0.9610 | Under hypoxic conditions, prolyl hydroxylation of HIF is inhibited, allowing it to escape ProteinVHL - mediated degradation. |
| Score | Text |
|---|---|
| 0.9959 | The transcriptional regulation of the Proteinerythropoietin gene by HIF raises the possibility that HIF may play a role in disorders of erythropoiesis, such as idiopathic erythrocytosis ( IE ). |
| Score | Text |
|---|---|
| 0.9998 | RESULTS : Patients with IE were screened for changes in the ProteinHIF - 1alpha coding sequence, and a change in the ODD domain that converts Pro - 582 to Ser was identified in several patients. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9946 | CONCLUSION : The Pro582Ser change represents a common polymorphism of ProteinHIF - 1alpha that does not impair HIF - 1alpha prolyl hydroxylation. |
| 0.9924 | CONCLUSION : The Pro582Ser change represents a common polymorphism of HIF - 1alpha that does not impair ProteinHIF - 1alpha prolyl hydroxylation. |
| 0.9489 | CONCLUSION : The Pro582Ser change represents a common polymorphism of HIF - 1alpha that does not impair HIF - 1alpha prolyl Hydroxylationhydroxylation . |
| 0.8726 | CONCLUSION : The Pro582Ser change represents a common polymorphism of HIF - 1alpha that does not impair HIF - 1alpha Entityprolyl hydroxylation. |
| Score | Text |
|---|---|
| 0.9993 | Although the Pro582Ser polymorphism is located in the ODD domain of HIF - 1alpha it does not diminish the association of HIF - 1alpha with ProteinVHL . |
| 0.9993 | Although the Pro582Ser polymorphism is located in the ODD domain of HIF - 1alpha it does not diminish the association of ProteinHIF - 1alpha with VHL. |
| 0.9988 | Although the Pro582Ser polymorphism is located in the ODD domain of ProteinHIF - 1alpha it does not diminish the association of HIF - 1alpha with VHL. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9959 | Expression of Proteinhistone acetyltransferases was down - regulated in poly ( ADP - ribose ) polymerase - 1 - deficient murine cells. |
| 0.9189 | Expression of histone acetyltransferases was down - regulated in Proteinpoly ( ADP - ribose ) polymerase - 1 - deficient murine cells. |
| Score | Text |
|---|---|
| 0.9774 | NF - kappaB - dependent, as well as human immunodeficiency virus type - 1 ( HIV - 1 ) long terminal repeat ( LTR ) - dependent, reporter gene expression was significantly impaired in cells derived from poly ( ADP - ribose ) polymerase - 1 ( PARP - 1 ) - knockout Protein( PARP - 1 - / - ) mice. |
| 0.8555 | NF - kappaB - dependent, as well as human immunodeficiency virus type - 1 ( HIV - 1 ) long terminal repeat ( LTR ) - dependent, reporter gene expression was significantly impaired in cells derived from Proteinpoly ( ADP - ribose ) polymerase - 1 ( PARP - 1 ) - knockout ( PARP - 1 - / - ) mice. |
| 0.9747 | NF - kappaB - dependent, as well as human immunodeficiency virus type - 1 ( HIV - 1 ) long terminal repeat ( LTR ) - dependent, reporter gene expression was significantly impaired in cells derived from poly ( ADP - ribose ) polymerase - 1 ( PARP - 1 ) - knockout Protein( PARP - 1 - / - ) mice. |
| 0.9455 | NF - kappaB - dependent, as well as human immunodeficiency virus type - 1 ( HIV - 1 ) long terminal repeat ( LTR ) - dependent, reporter gene expression was significantly impaired in cells derived from poly ( ADP - ribose ) polymerase - 1 ( PARP - 1 ) - knockout ( PARP - 1 Protein- / - ) mice. |
| NF - kappaB - dependent, as well as human immunodeficiency virus type - 1 ( HIV - 1 ) long terminal repeat ( LTR ) - dependent, reporter gene expression was significantly impaired in cells derived from poly ( ADP - ribose ) polymerase - 1 Protein( PARP - 1 ) - knockout ( PARP - 1 - / - ) mice. | |
| Score | Text |
|---|---|
| 0.9983 | In addition, the level of protein acetylation was markedly lower in ProteinPARP - 1 - / - cells than control ( PARP - 1 + / + ) cells. |
| 0.9866 | In addition, the level of protein acetylation was markedly lower in PARP - 1 - / - cells than control Protein( PARP - 1 + / + ) cells. |
| 0.5370 | In addition, the level of protein Acetylationacetylation was markedly lower in PARP - 1 - / - cells than control ( PARP - 1 + / + ) cells. |
| Score | Text |
|---|---|
| 0.9995 | Surprisingly, the expression levels of histone acetyltransferases ( HATs ), Proteinp300 , cAMP response element - binding protein - binding protein ( CBP ), and p300 / CBP - associated factor ( PCAF ), were significantly reduced in PARP - 1 - / - cells, as compared with PARP - 1 + / + cells. |
| 0.9991 | Surprisingly, the expression levels of histone acetyltransferases ( HATs ), p300, cAMP response element - binding protein - binding protein ( CBP ), and p300 / CBP - associated factor ( PCAF ), were significantly reduced in ProteinPARP - 1 - / - cells, as compared with PARP - 1 + / + cells. |
| 0.9990 | Surprisingly, the expression levels of histone acetyltransferases ( HATs ), p300, cAMP response element - binding protein - binding protein ( CBP ), and p300 / CBP - associated factor ( PCAF ), were significantly reduced in PARP - 1 - / - cells, as compared with ProteinPARP - 1 + / + cells. |
| 0.9936 | Surprisingly, the expression levels of histone acetyltransferases ( HATs ), p300, cAMP response element - binding protein - binding protein ( CBP ), and p300 / CBP - associated factor Protein( PCAF ) , were significantly reduced in PARP - 1 - / - cells, as compared with PARP - 1 + / + cells. |
| 0.9929 | Surprisingly, the expression levels of Proteinhistone acetyltransferases ( HATs ), p300, cAMP response element - binding protein - binding protein ( CBP ), and p300 / CBP - associated factor ( PCAF ), were significantly reduced in PARP - 1 - / - cells, as compared with PARP - 1 + / + cells. |
| 0.9807 | Surprisingly, the expression levels of histone acetyltransferases ( HATs ), p300, cAMP response element - binding protein - binding protein Protein( CBP ) , and p300 / CBP - associated factor ( PCAF ), were significantly reduced in PARP - 1 - / - cells, as compared with PARP - 1 + / + cells. |
| 0.9652 | Surprisingly, the expression levels of histone acetyltransferases ( HATs ), p300, cAMP response element - binding protein - binding protein ( CBP ), and Proteinp300 / CBP - associated factor ( PCAF ), were significantly reduced in PARP - 1 - / - cells, as compared with PARP - 1 + / + cells. |
| 0.8667 | Surprisingly, the expression levels of histone acetyltransferases ( HATs ), p300, ProteincAMP response element - binding protein - binding protein ( CBP ), and p300 / CBP - associated factor ( PCAF ), were significantly reduced in PARP - 1 - / - cells, as compared with PARP - 1 + / + cells. |
| 0.5825 | Surprisingly, the expression levels of histone acetyltransferases ( HATs ), p300, cAMP response element - binding protein - binding protein ( CBP ), and Proteinp300 / CBP - associated factor ( PCAF ) , were significantly reduced in PARP - 1 - / - cells, as compared with PARP - 1 + / + cells. |
| Score | Text |
|---|---|
| 0.9987 | These results suggest that ProteinPARP - 1 is required for the proper expression of particular HATs. |
| Score | Text |
|---|---|
| 0.9992 | Since p300 and CBP are coactivators of NF - kappaB, we propose here that ProteinPARP - 1 participates in NF - kappaB - dependent transcription by means of maintaining the expression of HATs. |
| 0.9989 | Since p300 and ProteinCBP are coactivators of NF - kappaB, we propose here that PARP - 1 participates in NF - kappaB - dependent transcription by means of maintaining the expression of HATs. |
| 0.9982 | Since Proteinp300 and CBP are coactivators of NF - kappaB, we propose here that PARP - 1 participates in NF - kappaB - dependent transcription by means of maintaining the expression of HATs. |
| Score | Text |
|---|---|
| 0.9693 | The ITIM - bearing ProteinCLECSF6 ( DCIR ) is down - modulated in neutrophils by neutrophil activating agents. |
| 0.9686 | The ITIM - bearing CLECSF6 Protein( DCIR ) is down - modulated in neutrophils by neutrophil activating agents. |
| Score | Text |
|---|---|
| 0.9996 | The recently discovered ProteinCLECSF6 protein displays the features of a receptor involved in the down - modulation of leukocyte activation. |
| Score | Text |
|---|---|
| 0.9984 | Although ProteinCLECSF6 has been the focus of the interest of many researchers lately, a Western blot characterization of the protein is still lacking. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9993 | Four different ProteinCLECSF6 mRNA species have been discovered to date. |
| Score | Text |
|---|---|
| 0.9986 | When deglycosylated, the protein displayed the molecular weight expected for the longest ProteinCLECSF6 form. |
| 0.4936 | When Deglycosylationdeglycosylated , the protein displayed the molecular weight expected for the longest CLECSF6 form. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9869 | We showed a down - modulation of the expression of this protein in neutrophils treated with granulocyte - macrophage - colony stimulating factor ( GM - CSF ), tumor necrosis factor Protein( TNF - alpha ) , lipopolysaccharide ( LPS ), and interleukin ( IL ) - 4. |
| 0.9723 | We showed a down - modulation of the expression of this protein in neutrophils treated with granulocyte - macrophage - colony stimulating factor Protein( GM - CSF ) , tumor necrosis factor ( TNF - alpha ), lipopolysaccharide ( LPS ), and interleukin ( IL ) - 4. |
| 0.9241 | We showed a down - modulation of the expression of this protein in neutrophils treated with granulocyte - macrophage - colony stimulating factor ( GM - CSF ), tumor necrosis factor ( TNF - alpha ), lipopolysaccharide ( LPS ), and Proteininterleukin ( IL ) - 4 . |
| 0.9057 | We showed a down - modulation of the expression of this protein in neutrophils treated with Proteingranulocyte - macrophage - colony stimulating factor ( GM - CSF ), tumor necrosis factor ( TNF - alpha ), lipopolysaccharide ( LPS ), and interleukin ( IL ) - 4. |
| 0.7893 | We showed a down - modulation of the expression of this protein in neutrophils treated with granulocyte - macrophage - colony stimulating factor ( GM - CSF ), Proteintumor necrosis factor ( TNF - alpha ), lipopolysaccharide ( LPS ), and interleukin ( IL ) - 4. |
| 0.8551 | We showed a down - modulation of the expression of this protein in neutrophils treated with granulocyte - macrophage - colony stimulating factor ( GM - CSF ), tumor necrosis factor ( TNF - alpha ), lipopolysaccharide ( LPS ), and interleukin Protein( IL ) - 4 . |
| Score | Text |
|---|---|
| 0.9997 | This work supports the hypothesis that ProteinCLECSF6 is involved in the control of inflammation in neutrophils. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9613 | Parental - silenced HeLo1 ( hemizygous for locus 1 ) plants show posttranscriptional silencing of the residing ProteinnptII ( neomycin phosphotransferase II ) transgene and cytosine methylation restricted to the 3'end and center part of the transcribed region. |
| 0.9420 | Parental - silenced HeLo1 ( hemizygous for locus 1 ) plants show posttranscriptional silencing of the residing nptII ( neomycin phosphotransferase II ) transgene and cytosine DNA_methylationmethylation restricted to the 3'end and center part of the transcribed region. |
| 0.7816 | Parental - silenced HeLo1 ( hemizygous for locus 1 ) plants show posttranscriptional silencing of the residing nptII ( neomycin phosphotransferase II ) transgene and cytosine methylation restricted to the Entity3'end and center part of the transcribed region. |
| 0.7225 | Parental - silenced HeLo1 ( hemizygous for locus 1 ) plants show posttranscriptional silencing of the residing nptII ( neomycin phosphotransferase II ) transgene and cytosine methylation restricted to the 3'end and Entitycenter part of the transcribed region. |
| 0.5416 | Parental - silenced HeLo1 ( hemizygous for locus 1 ) plants show posttranscriptional silencing of the residing nptII Protein( neomycin phosphotransferase II ) transgene and cytosine methylation restricted to the 3'end and center part of the transcribed region. |
| 0.7828 | Parental - silenced HeLo1 ( hemizygous for locus 1 ) plants show posttranscriptional silencing of the residing nptII ( neomycin phosphotransferase II ) transgene and cytosine methylation restricted to the 3 ' Entityend and center part of the transcribed region. |
| 0.7353 | Parental - silenced HeLo1 ( hemizygous for locus 1 ) plants show posttranscriptional silencing of the residing nptII ( neomycin phosphotransferase II ) transgene and cytosine methylation restricted to the Entity3 ' end and center part of the transcribed region. |
| 0.7227 | Parental - silenced HeLo1 ( hemizygous for locus 1 ) plants show posttranscriptional silencing of the residing nptII ( neomycin phosphotransferase II ) transgene and cytosine methylation restricted to the 3'end and Entitycenter part of the transcribed region. |
| 0.5820 | Parental - silenced HeLo1 ( hemizygous for locus 1 ) plants show posttranscriptional silencing of the residing ProteinnptII ( neomycin phosphotransferase II ) transgene and cytosine methylation restricted to the 3'end and center part of the transcribed region. |
| 0.5382 | Parental - silenced HeLo1 ( hemizygous for locus 1 ) plants show posttranscriptional silencing of the residing nptII ( neomycin phosphotransferase II ) transgene and cytosine methylation restricted to the 3'end and center part of the Entitytranscribed region . |
| Score | Text |
|---|---|
| 0.6076 | Here, we report that with an increasing number of cell cycles, DNA methylation changes gradually, and methylation is introduced into the Entitypromoter during cell culture and more slowly in vegetatively propagated plants. |
| Score | Text |
|---|---|
| 0.9740 | After 24 months of callus in vitro cultivation, an epigenetic variant, designated locus 1E, was obtained in which cytosine DNA_methylationmethylation of symmetrical ( CG and CNG ) sites was almost complete within the 5'end of the nptII - transcribed region and the 35S promoter. |
| 0.9654 | After 24 months of callus in vitro cultivation, an epigenetic variant, designated locus 1E, was obtained in which cytosine methylation of symmetrical ( CG and CNG ) sites was almost complete within the 5'end of the ProteinnptII - transcribed region and the 35S promoter. |
| 0.9293 | After 24 months of callus in vitro cultivation, an epigenetic variant, designated locus 1E, was obtained in which cytosine methylation of symmetrical ( CG and CNG ) sites was almost complete within the 5'end of the nptII - transcribed region and the Entity35S promoter . |
| 0.8839 | After 24 months of callus in vitro cultivation, an epigenetic variant, designated locus 1E, was obtained in which cytosine methylation of symmetrical ( CG and CNG ) sites was almost complete within the Entity5'end of the nptII - transcribed region and the 35S promoter. |
| 0.9458 | After 24 months of callus in vitro cultivation, an epigenetic variant, designated locus 1E, was obtained in which cytosine methylation of symmetrical ( CG and CNG ) sites was almost complete within the 5'end of the nptII - transcribed region and the 35S Entitypromoter . |
| 0.9054 | After 24 months of callus in vitro cultivation, an epigenetic variant, designated locus 1E, was obtained in which cytosine methylation of symmetrical ( CG and CNG ) sites was almost complete within the Entity5 ' end of the nptII - transcribed region and the 35S promoter. |
| 0.8944 | After 24 months of callus in vitro cultivation, an epigenetic variant, designated locus 1E, was obtained in which cytosine methylation of symmetrical ( CG and CNG ) sites was almost complete within the 5'end of the nptII - transcribed region and the Entity35S promoter. |
| 0.6277 | After 24 months of callus in vitro cultivation, an epigenetic variant, designated locus 1E, was obtained in which cytosine methylation of symmetrical ( CG and CNG ) sites was almost complete within the 5 ' Entityend of the nptII - transcribed region and the 35S promoter. |
| 0.5728 | After 24 months of callus in vitro cultivation, an epigenetic variant, designated locus 1E, was obtained in which cytosine methylation of symmetrical ( CG and CNG ) sites was almost complete within the 5'end of the nptII - transcribed Entityregion and the 35S promoter. |
| Score | Text |
|---|---|
| 0.9692 | Further, DNA_methylationmethylation of nonsymmetrical sites appeared de novo in the promoter, whereas this type of methylation was significantly reduced in the 3'end of the transcribed region when compared with locus 1. |
| 0.8032 | Further, methylation of nonsymmetrical sites appeared de novo in the promoter, whereas this type of methylation was significantly reduced in the 3'end of the Entitytranscribed region when compared with locus 1. |
| 0.7896 | Further, methylation of nonsymmetrical sites appeared de novo in the Entitypromoter , whereas this type of methylation was significantly reduced in the 3'end of the transcribed region when compared with locus 1. |
| 0.9536 | Further, methylation of nonsymmetrical sites appeared de novo in the promoter, whereas this type of DNA_methylationmethylation was significantly reduced in the 3'end of the transcribed region when compared with locus 1. |
| 0.6352 | Further, methylation of nonsymmetrical sites appeared de novo in the promoter, whereas this type of methylation was significantly reduced in the 3'end of the Entitytranscribed region when compared with locus 1. |
| 0.5083 | Further, methylation of nonsymmetrical sites appeared de novo in the promoter, whereas this type of methylation was significantly reduced in the Entity3 ' end of the transcribed region when compared with locus 1. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9989 | The protein and steady - state RNA levels remained low in locus 1E, whereas with nuclear run - on assays, no detectable amounts of primary transcripts were found along the ProteinnptII gene, indicating that the methylated promoter became inactivated. |
| 0.9927 | The protein and steady - state RNA levels remained low in locus 1E, whereas with nuclear run - on assays, no detectable amounts of primary transcripts were found along the nptII gene, indicating that the methylated Entitypromoter became inactivated. |
| 0.9706 | The protein and steady - state RNA levels remained low in locus 1E, whereas with nuclear run - on assays, no detectable amounts of primary transcripts were found along the nptII gene, indicating that the DNA_methylationmethylated promoter became inactivated. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9968 | Frequent methylation of p16INK4A and Proteinp14ARF genes implicated in the evolution of chronic myeloid leukaemia from its chronic to accelerated phase. |
| 0.9966 | Frequent methylation of Proteinp16INK4A and p14ARF genes implicated in the evolution of chronic myeloid leukaemia from its chronic to accelerated phase. |
| 0.8214 | Frequent DNA_methylationmethylation of p16INK4A and p14ARF genes implicated in the evolution of chronic myeloid leukaemia from its chronic to accelerated phase. |
| Score | Text |
|---|---|
| 0.9971 | The frequency and mechanism of p16 ( INK4A ) and Proteinp14 ( ARF ) gene alterations were studied in cell samples from 30 patients with Philadelphia ( Ph ) chromosome - positive chronic myeloid leukaemia ( CML ), both at diagnosis and at the onset of the accelerated phase ( AP ) of the disease. |
| 0.9964 | The frequency and mechanism of Proteinp16 ( INK4A ) and p14 ( ARF ) gene alterations were studied in cell samples from 30 patients with Philadelphia ( Ph ) chromosome - positive chronic myeloid leukaemia ( CML ), both at diagnosis and at the onset of the accelerated phase ( AP ) of the disease. |
| Score | Text |
|---|---|
| 0.9950 | No alterations in the Proteinp16 ( INK4A ) or p14 ( ARF ) genes were found in any of the chronic phase ( CP ) samples. |
| 0.9935 | No alterations in the p16 ( INK4A ) or Proteinp14 ( ARF ) genes were found in any of the chronic phase ( CP ) samples. |
| Score | Text |
|---|---|
| 0.9970 | DNA sequencing analyses detected Proteinp16 ( INK4A ) or p14 ( ARF ) mutations in 17 AP samples. |
| 0.9970 | DNA sequencing analyses detected p16 ( INK4A ) or Proteinp14 ( ARF ) mutations in 17 AP samples. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9930 | Aberrant DNA_methylationmethylation of the p16 ( INK4A ) or p14 ( ARF ) promoters was found in 14 of 30 AP samples. |
| 0.9839 | Aberrant methylation of the p16 ( INK4A ) or Proteinp14 ( ARF ) promoters was found in 14 of 30 AP samples. |
| 0.9797 | Aberrant methylation of the Proteinp16 ( INK4A ) or p14 ( ARF ) promoters was found in 14 of 30 AP samples. |
| 0.9729 | Aberrant methylation of the p16 ( INK4A ) or p14 ( ARF ) Entitypromoters was found in 14 of 30 AP samples. |
| Score | Text |
|---|---|
| 0.9765 | The most common situation was the simultaneous methylation of both Entitypromoters . |
| 0.9643 | The most common situation was the simultaneous DNA_methylationmethylation of both promoters. |
| Score | Text |
|---|---|
| 0.9933 | Our data indicate that p16 ( INK4A ) and Proteinp14 ( ARF ) are primary targets for inactivation by promoter methylation in the acceleration of CML. |
| 0.9919 | Our data indicate that Proteinp16 ( INK4A ) and p14 ( ARF ) are primary targets for inactivation by promoter methylation in the acceleration of CML. |
| 0.9915 | Our data indicate that p16 ( INK4A ) and p14 ( ARF ) are primary targets for inactivation by Entitypromoter methylation in the acceleration of CML. |
| 0.9585 | Our data indicate that p16 ( INK4A ) and p14 ( ARF ) are primary targets for inactivation by promoter DNA_methylationmethylation in the acceleration of CML. |
| Score | Text |
|---|---|
| 0.9957 | Transcriptional silencing of the Proteinp16 ( INK4A ) and p14 ( ARF ) genes may be important in the conversion of CML from the CP to the AP. |
| 0.9926 | Transcriptional silencing of the p16 ( INK4A ) and Proteinp14 ( ARF ) genes may be important in the conversion of CML from the CP to the AP. |
| Score | Text |
|---|---|
| 0.9996 | mSin3A / histone deacetylase 2 - and PRMT5 - containing Brg1 complex is involved in transcriptional repression of the Myc target gene Proteincad . |
| 0.9996 | mSin3A / histone deacetylase 2 - and PRMT5 - containing Brg1 complex is involved in transcriptional repression of the ProteinMyc target gene cad. |
| 0.9763 | ProteinmSin3A / histone deacetylase 2 - and PRMT5 - containing Brg1 complex is involved in transcriptional repression of the Myc target gene cad. |
| 0.9317 | mSin3A / histone deacetylase 2 - and PRMT5 - containing ProteinBrg1 complex is involved in transcriptional repression of the Myc target gene cad. |
| 0.7093 | ProteinmSin3A / histone deacetylase 2 - and PRMT5 - containing Brg1 complex is involved in transcriptional repression of the Myc target gene cad. |
| 0.6314 | mSin3A / histone deacetylase 2 - and ProteinPRMT5 - containing Brg1 complex is involved in transcriptional repression of the Myc target gene cad. |
| 0.7867 | mSin3A / histone deacetylase 2 - and ProteinPRMT5 - containing Brg1 complex is involved in transcriptional repression of the Myc target gene cad. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9715 | We have previously shown that subunits of the mSin3A / histone deacetylase 2 Protein( HDAC2 ) corepressor complex copurify with hSWI / SNF complexes. |
| 0.9288 | We have previously shown that subunits of the ProteinmSin3A / histone deacetylase 2 ( HDAC2 ) corepressor complex copurify with hSWI / SNF complexes. |
| 0.6487 | We have previously shown that subunits of the ProteinmSin3A / histone deacetylase 2 ( HDAC2 ) corepressor complex copurify with hSWI / SNF complexes. |
| Score | Text |
|---|---|
| 0.9999 | Here we show that the type II arginine - specific methyltransferase ProteinPRMT5 , which is involved in cyclin E repression, can be found in association with Brg1 and hBrm - based hSWI / SNF complexes. |
| 0.9998 | Here we show that the type II arginine - specific methyltransferase PRMT5, which is involved in cyclin E repression, can be found in association with ProteinBrg1 and hBrm - based hSWI / SNF complexes. |
| 0.9986 | Here we show that the type II arginine - specific methyltransferase PRMT5, which is involved in cyclin E repression, can be found in association with Brg1 and ProteinhBrm - based hSWI / SNF complexes. |
| 0.7728 | Here we show that the type II arginine - specific methyltransferase PRMT5, which is involved in Proteincyclin E repression, can be found in association with Brg1 and hBrm - based hSWI / SNF complexes. |
| Score | Text |
|---|---|
| 0.9889 | We also show that hSWI / SNF - associated ProteinPRMT5 can methylate hypoacetylated histones H3 and H4 more efficiently than hyperacetylated histones H3 and H4. |
| 0.9673 | We also show that hSWI / SNF - associated PRMT5 can methylate hypoacetylated histones H3 and ProteinH4 more efficiently than hyperacetylated histones H3 and H4. |
| 0.9507 | We also show that hSWI / SNF - associated PRMT5 can methylate hypoacetylated histones H3 and H4 more efficiently than hyperacetylated histones H3 and ProteinH4 . |
| 0.8992 | We also show that hSWI / SNF - associated PRMT5 can methylate hypoacetylated Proteinhistones H3 and H4 more efficiently than hyperacetylated histones H3 and H4. |
| 0.8981 | We also show that hSWI / SNF - associated PRMT5 can methylate hypoacetylated histones H3 and H4 more efficiently than Acetylationhyperacetylated histones H3 and H4. |
| 0.8859 | We also show that hSWI / SNF - associated PRMT5 can methylate hypoacetylated histones H3 and H4 more efficiently than hyperacetylated Proteinhistones H3 and H4. |
| 0.5522 | We also show that hSWI / SNF - associated PRMT5 can Methylationmethylate hypoacetylated histones H3 and H4 more efficiently than hyperacetylated histones H3 and H4. |
| 0.8602 | We also show that hSWI / SNF - associated PRMT5 can methylate Acetylationhypoacetylated histones H3 and H4 more efficiently than hyperacetylated histones H3 and H4. |
| 0.4086 | We also show that hSWI / SNF - associated PRMT5 can Acetylationmethylate hypoacetylated histones H3 and H4 more efficiently than hyperacetylated histones H3 and H4. |
| We also show that hSWI / SNF - associated PRMT5 can Catalysismethylate hypoacetylated histones H3 and H4 more efficiently than hyperacetylated histones H3 and H4. | |
| We also show that hSWI / SNF - associated PRMT5 can methylate Deacetylationhypoacetylated histones H3 and H4 more efficiently than hyperacetylated histones H3 and H4. | |
| Score | Text |
|---|---|
| 0.9998 | Protein - protein interaction studies indicate that PRMT5 and mSin3A interact with the same hSWI / SNF subunits as those targeted by Proteinc - Myc . |
| 0.9997 | Protein - protein interaction studies indicate that ProteinPRMT5 and mSin3A interact with the same hSWI / SNF subunits as those targeted by c - Myc. |
| 0.9996 | Protein - protein interaction studies indicate that PRMT5 and ProteinmSin3A interact with the same hSWI / SNF subunits as those targeted by c - Myc. |
| Score | Text |
|---|---|
| 0.9995 | These observations prompted us to examine the expression profile of the Proteinc - Myc target genes, carbamoyl - phosphate synthase - aspartate carbamoyltransferase - dihydroorotase ( cad ) and nucleolin ( nuc ). |
| 0.9893 | These observations prompted us to examine the expression profile of the c - Myc target genes, carbamoyl - phosphate synthase - aspartate carbamoyltransferase - dihydroorotase Protein( cad ) and nucleolin ( nuc ). |
| 0.9884 | These observations prompted us to examine the expression profile of the c - Myc target genes, carbamoyl - phosphate synthase - aspartate carbamoyltransferase - dihydroorotase ( cad ) and nucleolin Protein( nuc ) . |
| 0.8008 | These observations prompted us to examine the expression profile of the c - Myc target genes, Proteincarbamoyl - phosphate synthase - aspartate carbamoyltransferase - dihydroorotase ( cad ) and nucleolin ( nuc ). |
| 0.7198 | These observations prompted us to examine the expression profile of the c - Myc target genes, carbamoyl - phosphate synthase - aspartate carbamoyltransferase - dihydroorotase ( cad ) and Proteinnucleolin ( nuc ). |
| 0.6112 | These observations prompted us to examine the expression profile of the c - Myc target genes, carbamoyl - phosphate synthase - aspartate Proteincarbamoyltransferase - dihydroorotase ( cad ) and nucleolin ( nuc ). |
| 0.5662 | These observations prompted us to examine the expression profile of the c - Myc target genes, carbamoyl - phosphate Proteinsynthase - aspartate carbamoyltransferase - dihydroorotase ( cad ) and nucleolin ( nuc ). |
| 0.7418 | These observations prompted us to examine the expression profile of the c - Myc target genes, Proteincarbamoyl - phosphate synthase - aspartate carbamoyltransferase - dihydroorotase ( cad ) and nucleolin ( nuc ). |
| 0.5126 | These observations prompted us to examine the expression profile of the c - Myc target genes, carbamoyl - phosphate Proteinsynthase - aspartate carbamoyltransferase - dihydroorotase ( cad ) and nucleolin ( nuc ). |
| Score | Text |
|---|---|
| 0.9998 | We found that Proteincad repression is altered in cells that express inactive Brg1 and in cells treated with the HDAC inhibitor depsipeptide. |
| 0.9997 | We found that cad repression is altered in cells that express inactive ProteinBrg1 and in cells treated with the HDAC inhibitor depsipeptide. |
| Score | Text |
|---|---|
| 0.9998 | Using chromatin immunoprecipitation assays, we found that Brg1, mSin3A, HDAC2, and ProteinPRMT5 are directly recruited to the cad promoter. |
| 0.9996 | Using chromatin immunoprecipitation assays, we found that Brg1, mSin3A, ProteinHDAC2 , and PRMT5 are directly recruited to the cad promoter. |
| 0.9995 | Using chromatin immunoprecipitation assays, we found that Brg1, ProteinmSin3A , HDAC2, and PRMT5 are directly recruited to the cad promoter. |
| 0.9994 | Using chromatin immunoprecipitation assays, we found that ProteinBrg1 , mSin3A, HDAC2, and PRMT5 are directly recruited to the cad promoter. |
| 0.9967 | Using chromatin immunoprecipitation assays, we found that Brg1, mSin3A, HDAC2, and PRMT5 are directly recruited to the Proteincad promoter. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9651 | Centromere silencing and function in fission yeast is governed by the amino terminus of Proteinhistone H3 . |
| Score | Text |
|---|---|
| 0.9866 | BACKGROUND : Centromeric domains often consist of repetitive elements that are assembled in specialized chromatin, characterized by hypoacetylation of histones H3 and ProteinH4 and methylation of lysine 9 of histone H3 ( K9 - MeH3 ). |
| 0.9522 | BACKGROUND : Centromeric domains often consist of repetitive elements that are assembled in specialized chromatin, characterized by hypoacetylation of histones H3 and H4 and Methylationmethylation of lysine 9 of histone H3 ( K9 - MeH3 ). |
| 0.9332 | BACKGROUND : Centromeric domains often consist of repetitive elements that are assembled in specialized chromatin, characterized by hypoacetylation of Proteinhistones H3 and H4 and methylation of lysine 9 of histone H3 ( K9 - MeH3 ). |
| 0.9282 | BACKGROUND : Centromeric domains often consist of repetitive elements that are assembled in specialized chromatin, characterized by hypoacetylation of histones H3 and H4 and methylation of lysine 9 of Proteinhistone H3 ( K9 - MeH3 ). |
| 0.9264 | BACKGROUND : Centromeric domains often consist of repetitive elements that are assembled in specialized chromatin, characterized by Acetylationhypoacetylation of histones H3 and H4 and methylation of lysine 9 of histone H3 ( K9 - MeH3 ). |
| 0.8943 | BACKGROUND : Centromeric domains often consist of repetitive elements that are assembled in specialized chromatin, characterized by hypoacetylation of histones H3 and H4 and methylation of Entitylysine 9 of histone H3 ( K9 - MeH3 ). |
| 0.5115 | BACKGROUND : Centromeric domains often consist of repetitive elements that are assembled in specialized chromatin, characterized by hypoacetylation of histones H3 and H4 and methylation of lysine 9 of histone H3 Entity( K9 - MeH3 ) . |
| 0.5391 | BACKGROUND : Centromeric domains often consist of repetitive elements that are assembled in specialized chromatin, characterized by hypoacetylation of histones H3 and H4 and methylation of Entitylysine 9 of histone H3 ( K9 - MeH3 ). |
| BACKGROUND : Centromeric domains often consist of repetitive elements that are assembled in specialized chromatin, characterized by hypoacetylation of histones H3 and H4 and methylation of lysine 9 of histone H3 Protein( K9 - MeH3 ) . | |
| Score | Text |
|---|---|
| 0.9991 | Perturbation of this underacetylated state by transient treatment with histone deacetylase inhibitors leads to defective centromere function, correlating with delocalization of the heterochromatin protein ProteinSwi6 / HP1 . |
| 0.9987 | Perturbation of this underacetylated state by transient treatment with Proteinhistone deacetylase inhibitors leads to defective centromere function, correlating with delocalization of the heterochromatin protein Swi6 / HP1. |
| Score | Text |
|---|---|
| 0.9987 | Likewise, deletion of the K9 - MeH3 methyltransferase ProteinClr4 / Suvar39 causes defective chromosome segregation. |
| 0.9893 | Likewise, deletion of the ProteinK9 - MeH3 methyltransferase Clr4 / Suvar39 causes defective chromosome segregation. |
| Score | Text |
|---|---|
| 0.9995 | Here, we create fission yeast strains retaining one histone H3 and ProteinH4 gene ; the creation of these strains allows mutation of specific N - terminal tail residues and their role in centromeric silencing and chromosome stability to be investigated. |
| 0.9899 | Here, we create fission yeast strains retaining one Proteinhistone H3 and H4 gene ; the creation of these strains allows mutation of specific N - terminal tail residues and their role in centromeric silencing and chromosome stability to be investigated. |
| Score | Text |
|---|---|
| 0.9993 | RESULTS : Reduction of ProteinH3 / H4 gene dosage to one - third does not affect cell viability or heterochromatin formation. |
| Score | Text |
|---|---|
| 0.9994 | Mutation of lysines 9 or 14 or serine 10 within the amino terminus of histone H3 impairs centromere function, leading to defective chromosome segregation and ProteinSwi6 delocalization. |
| 0.9658 | Mutation of lysines 9 or 14 or serine 10 within the amino terminus of Proteinhistone H3 impairs centromere function, leading to defective chromosome segregation and Swi6 delocalization. |
| Score | Text |
|---|---|
| 0.9723 | Surprisingly, silent centromeric chromatin does not require the conserved lysine 8 and 16 residues of Proteinhistone H4 . |
| Score | Text |
|---|---|
| 0.9989 | CONCLUSIONS : To date, mutation of conserved N - terminal residues in endogenous histone genes has only been performed in budding yeast, which lacks the Clr4 / Suvar39 histone methyltransferase and ProteinSwi6 / HP1 . |
| 0.9976 | CONCLUSIONS : To date, mutation of conserved N - terminal residues in endogenous Proteinhistone genes has only been performed in budding yeast, which lacks the Clr4 / Suvar39 histone methyltransferase and Swi6 / HP1. |
| 0.9228 | CONCLUSIONS : To date, mutation of conserved N - terminal residues in endogenous histone genes has only been performed in budding yeast, which lacks the ProteinClr4 / Suvar39 histone methyltransferase and Swi6 / HP1. |
| Score | Text |
|---|---|
| 0.9839 | We demonstrate the importance of conserved residues within the Proteinhistone H3 N terminus for the maintenance of centromeric heterochromatin in fission yeast. |
| Score | Text |
|---|---|
| 0.9493 | In sharp contrast, mutation of two conserved lysines within the Proteinhistone H4 tail has no impact on the integrity of centromeric heterochromatin. |
| Score | Text |
|---|---|
| 0.9949 | Our data highlight the striking divergence between the Proteinhistone tail requirements for the fission yeast and budding yeast silencing pathways. |
| Score | Text |
|---|---|
| 0.9844 | Thermal stability and aggregation of sulfolobus solfataricus Proteinbeta - glycosidase are dependent upon the N - epsilon - methylation of specific lysyl residues : critical role of in vivo post - translational modifications. |
| 0.9442 | Thermal stability and aggregation of sulfolobus solfataricus beta - glycosidase are dependent upon the N - epsilon - methylation of specific Entitylysyl residues : critical role of in vivo post - translational modifications. |
| 0.6472 | Thermal stability and aggregation of sulfolobus solfataricus beta - glycosidase are dependent upon the MethylationN - epsilon - methylation of specific lysyl residues : critical role of in vivo post - translational modifications. |
| 0.8880 | Thermal stability and aggregation of sulfolobus solfataricus beta - glycosidase are dependent upon the N - epsilon - methylation of specific Entitylysyl residues : critical role of in vivo post - translational modifications. |
| Score | Text |
|---|---|
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| 0.9784 | The aim of this work is to clarify some effects of methylation on the properties of beta - glycosidase from Sulfolobus solfataricus, by a structural comparison between the native, Methylationmethylated protein and its unmethylated counterpart, recombinantly expressed in Escherichia coli. |
| 0.9692 | The aim of this work is to clarify some effects of methylation on the properties of Proteinbeta - glycosidase from Sulfolobus solfataricus, by a structural comparison between the native, methylated protein and its unmethylated counterpart, recombinantly expressed in Escherichia coli. |
| 0.9608 | The aim of this work is to clarify some effects of methylation on the properties of beta - glycosidase from Sulfolobus solfataricus, by a structural comparison between the native, methylated protein and its Methylationunmethylated counterpart, recombinantly expressed in Escherichia coli. |
| 0.9157 | The aim of this work is to clarify some effects of Methylationmethylation on the properties of beta - glycosidase from Sulfolobus solfataricus, by a structural comparison between the native, methylated protein and its unmethylated counterpart, recombinantly expressed in Escherichia coli. |
| Score | Text |
|---|---|
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| 0.9969 | However, the study of temperature perturbation by Fourier transform infrared spectroscopy and turbidimetry evidenced denaturation and aggregation events more pronounced in recombinant than in native Proteinbeta - glycosidase . |
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| 0.9915 | A computational analysis of Proteinbeta - glycosidase three - dimensional structure and comparisons with other proteins from S. solfataricus revealed analogies in the localization of methylation sites in terms of secondary structural elements and overall topology. |
| Score | Text |
|---|---|
| 0.9913 | These observations suggest a role for the methylation of lysyl residues, located in selected domains, in the thermal stabilization of Proteinbeta - glycosidase from S. solfataricus. |
| 0.9567 | These observations suggest a role for the Methylationmethylation of lysyl residues, located in selected domains, in the thermal stabilization of beta - glycosidase from S. solfataricus. |
| 0.9143 | These observations suggest a role for the methylation of Entitylysyl residues , located in selected domains, in the thermal stabilization of beta - glycosidase from S. solfataricus. |
| 0.6708 | These observations suggest a role for the methylation of Entitylysyl residues, located in selected domains, in the thermal stabilization of beta - glycosidase from S. solfataricus. |
| Score | Text |
|---|---|
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| 0.9632 | Two pathways for PC biosynthesis are known in bacteria, the methylation pathway and the phosphatidylcholine synthase Protein( PCS ) pathway. |
| 0.8586 | Two pathways for PC biosynthesis are known in bacteria, the methylation pathway and the Proteinphosphatidylcholine synthase ( PCS ) pathway. |
| Score | Text |
|---|---|
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|---|---|
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| 0.9990 | Using cell - free extracts, it was demonstrated that Sinorhizobium meliloti, Agrobacterium tumefaciens, Rhizobium leguminosarum, Bradyrhizobium japonicum, Mesorhizobium loti and Legionella pneumophila have both PMT and ProteinPCS activities. |
| 0.9123 | Using cell - free extracts, it was demonstrated that Sinorhizobium meliloti, Agrobacterium tumefaciens, Rhizobium leguminosarum, Bradyrhizobium japonicum, Mesorhizobium loti and Legionella pneumophila have both ProteinPMT and PCS activities. |
| Score | Text |
|---|---|
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|---|---|
| 0.9995 | Genes from M. loti and L. pneumophila encoding a ProteinPmt or a Pcs activity and the genes from P. aeruginosa and Borrelia burgdorferi responsible for Pcs activity have been identified. |
| 0.9987 | Genes from M. loti and L. pneumophila encoding a Pmt or a Pcs activity and the genes from P. aeruginosa and Borrelia burgdorferi responsible for ProteinPcs activity have been identified. |
| 0.9986 | Genes from M. loti and L. pneumophila encoding a Pmt or a ProteinPcs activity and the genes from P. aeruginosa and Borrelia burgdorferi responsible for Pcs activity have been identified. |
| Score | Text |
|---|---|
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| 0.9992 | However, important pathogens such as Brucella melitensis, P. aeruginosa and Borrelia burgdorferi seem to be exceptional as they possess only the ProteinPCS pathway for PC formation. |
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|---|---|
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| 0.9858 | To validate our method, the product of human thiopurine methyltransferase Protein( TPMT , EC 2. 1. 1. 67 ) has been successfully identified from both an in vitro assay and a whole - cell assay. |
| 0.9026 | To validate our method, the product of human Proteinthiopurine methyltransferase ( TPMT, EC 2. 1. 1. 67 ) has been successfully identified from both an in vitro assay and a whole - cell assay. |
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|---|---|
| 0.9297 | Further analysis, including concanavalin A Protein( Con A ) affinity chromatography, desialylation, desulphation, sequential exoglycosidase digestion and methylation, clarified the structures of the acidic oligosaccharides. |
| 0.9002 | Further analysis, including Proteinconcanavalin A ( Con A ) affinity chromatography, desialylation, desulphation, sequential exoglycosidase digestion and methylation, clarified the structures of the acidic oligosaccharides. |
| 0.7227 | Further analysis, including concanavalin A Protein( Con A ) affinity chromatography, desialylation, desulphation, sequential exoglycosidase digestion and methylation, clarified the structures of the acidic oligosaccharides. |
| 0.5534 | Further analysis, including concanavalin A ( Con ProteinA ) affinity chromatography, desialylation, desulphation, sequential exoglycosidase digestion and methylation, clarified the structures of the acidic oligosaccharides. |
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|---|---|
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|---|---|
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|---|---|
| 0.9942 | The ProteinMTHFR 677C > T polymorphism is associated with an increased risk of hepatocellular carcinoma in patients with alcoholic cirrhosis. |
| Score | Text |
|---|---|
| 0.9879 | Methylenetetrahydrofolate reductase Protein( MTHFR ) , a key enzyme in folate metabolism, plays a major role in the provision of methyl groups for DNA methylation and in the production of dTMP for DNA synthesis. |
| 0.9147 | ProteinMethylenetetrahydrofolate reductase ( MTHFR ), a key enzyme in folate metabolism, plays a major role in the provision of methyl groups for DNA methylation and in the production of dTMP for DNA synthesis. |
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|---|---|
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|---|---|
| 0.9994 | The aim of this study was to determine whether the ProteinMTHFR polymorphism is related to hepatocellular carcinoma ( HCC ) in patients with alcoholic cirrhosis. |
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|---|---|
| 0.9995 | ProteinMTHFR genotypes were determined in 300 liver transplant patients, 72 of whom had alcoholic cirrhosis with HCC and 122 of whom had alcoholic cirrhosis without HCC. |
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|---|---|
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| 0.9994 | Among the group of patients transplanted for alcoholic cirrhosis, the frequency of ProteinMTHFR variants CC versus CT and TT was significantly higher in patients with HCC than in patients without macroscopic evidence of HCC ( P = 0. 02 ). |
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|---|---|
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| 0.9975 | If we considered all the patients transplanted for HCC, the ProteinMTHFR CC genotype was significantly higher in patients who had developed HCC on alcoholic cirrhosis rather than on viral cirrhosis ( P = 0. 002 ) or on non - cirrhotic livers ( P = 0. 02 ). |
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|---|---|
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| 0.9920 | These results suggest that the ProteinMTHFR CC genotype increases the risk to develop HCC in patients who consume a high alcohol diet. |
| Score | Text |
|---|---|
| 0.9998 | ProteinMbd1 is recruited to both methylated and nonmethylated CpGs via distinct DNA binding domains. |
| Score | Text |
|---|---|
| 0.9998 | ProteinMBD1 is a vertebrate methyl - CpG binding domain protein ( MBD ) that can bring about repression of methylated promoter DNA sequences. |
| Score | Text |
|---|---|
| 0.9999 | Like other MBD proteins, ProteinMBD1 localizes to nuclear foci that in mice are rich in methyl - CpG. |
| Score | Text |
|---|---|
| 0.9998 | In methyl - CpG - deficient mouse cells, however, ProteinMbd1 remains localized to heterochromatic foci whereas other MBD proteins become dispersed in the nucleus. |
| Score | Text |
|---|---|
| 0.9997 | We find that ProteinMbd1a , a major mouse isoform, contains a CXXC domain ( CXXC - 3 ) that binds specifically to nonmethylated CpG, suggesting an explanation for methylation - independent localization. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9998 | Our findings indicate that ProteinMBD1 can interpret the CpG dinucleotide as a repressive signal in vivo regardless of its methylation status. |
| Score | Text |
|---|---|
| 0.9996 | Recombinant human zona pellucida proteins ZP1, ZP2 and ProteinZP3 co - expressed in a human cell line. |
| 0.9995 | Recombinant human zona pellucida proteins ZP1, ProteinZP2 and ZP3 co - expressed in a human cell line. |
| 0.9994 | Recombinant human zona pellucida proteins ProteinZP1 , ZP2 and ZP3 co - expressed in a human cell line. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9998 | METHODS : The human embryonic kidney cell line 293T was employed to produce rhZP1, ProteinrhZP2 and rhZP3 proteins individually and together by co - expression. |
| 0.9997 | METHODS : The human embryonic kidney cell line 293T was employed to produce ProteinrhZP1 , rhZP2 and rhZP3 proteins individually and together by co - expression. |
| 0.9994 | METHODS : The human embryonic kidney cell line 293T was employed to produce rhZP1, rhZP2 and ProteinrhZP3 proteins individually and together by co - expression. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9997 | RESULTS : RhZP2 and rhZP3 were secreted into the culture medium, whereas ProteinrhZP1 was found only in the cell lysate. |
| 0.9995 | RESULTS : RhZP2 and ProteinrhZP3 were secreted into the culture medium, whereas rhZP1 was found only in the cell lysate. |
| 0.9993 | RESULTS : ProteinRhZP2 and rhZP3 were secreted into the culture medium, whereas rhZP1 was found only in the cell lysate. |
| Score | Text |
|---|---|
| 0.9998 | Interestingly, when all zona pellucida proteins were co - expressed in the same cells, ProteinrhZP1 was also secreted into the culture medium. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9992 | CONCLUSION : RhZP1, ProteinrhZP2 and rhZP3 were successfully expressed in the human embryonic kidney cell line 293T. |
| 0.9991 | CONCLUSION : RhZP1, rhZP2 and ProteinrhZP3 were successfully expressed in the human embryonic kidney cell line 293T. |
| 0.9983 | CONCLUSION : ProteinRhZP1 , rhZP2 and rhZP3 were successfully expressed in the human embryonic kidney cell line 293T. |
| Score | Text |
|---|---|
| 0.9999 | It appears that an interaction amongst these proteins may be required for release of ProteinrhZP1 from the cell. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9983 | Leu - 574 of human ProteinHIF - 1alpha is a molecular determinant of prolyl hydroxylation. |
| Score | Text |
|---|---|
| ProteinHypoxia - inducible factor ( HIF ) - 1alpha , a master regulator of oxygen homeostasis, regulates genes crucial for cell growth and survival. | |
| Score | Text |
|---|---|
| 0.9986 | In normoxia, ProteinHIF - 1alpha is constantly degraded via the ubiquitin - proteasome pathway. |
| 0.9977 | In normoxia, HIF - 1alpha is constantly degraded via the Proteinubiquitin - proteasome pathway. |
| Score | Text |
|---|---|
| 0.9993 | The von Hippel - Lindau ( VHL ) E3 ubiquitin ligase binds ProteinHIF - 1alpha through specific recognition of hydroxylated Pro - 402 or Pro - 564, both of which are modified by the oxygen - dependent HIF prolyl hydroxylases ( PHDs / HPHs ). |
| 0.9910 | The von Hippel - Lindau ( VHL ) E3 ubiquitin ligase binds HIF - 1alpha through specific recognition of hydroxylated Pro - 402 or EntityPro - 564 , both of which are modified by the oxygen - dependent HIF prolyl hydroxylases ( PHDs / HPHs ). |
| 0.9771 | The von Hippel - Lindau ( VHL ) E3 ubiquitin ligase binds HIF - 1alpha through specific recognition of hydroxylated EntityPro - 402 or Pro - 564, both of which are modified by the oxygen - dependent HIF prolyl hydroxylases ( PHDs / HPHs ). |
| 0.9660 | The von Hippel - Lindau ( VHL ) E3 Proteinubiquitin ligase binds HIF - 1alpha through specific recognition of hydroxylated Pro - 402 or Pro - 564, both of which are modified by the oxygen - dependent HIF prolyl hydroxylases ( PHDs / HPHs ). |
| 0.9576 | The von Hippel - Lindau ( VHL ) E3 ubiquitin ligase binds HIF - 1alpha through specific recognition of Hydroxylationhydroxylated Pro - 402 or Pro - 564, both of which are modified by the oxygen - dependent HIF prolyl hydroxylases ( PHDs / HPHs ). |
| 0.9187 | The von Hippel - Lindau Protein( VHL ) E3 ubiquitin ligase binds HIF - 1alpha through specific recognition of hydroxylated Pro - 402 or Pro - 564, both of which are modified by the oxygen - dependent HIF prolyl hydroxylases ( PHDs / HPHs ). |
| 0.7938 | The Proteinvon Hippel - Lindau ( VHL ) E3 ubiquitin ligase binds HIF - 1alpha through specific recognition of hydroxylated Pro - 402 or Pro - 564, both of which are modified by the oxygen - dependent HIF prolyl hydroxylases ( PHDs / HPHs ). |
| 0.5841 | The von ProteinHippel - Lindau ( VHL ) E3 ubiquitin ligase binds HIF - 1alpha through specific recognition of hydroxylated Pro - 402 or Pro - 564, both of which are modified by the oxygen - dependent HIF prolyl hydroxylases ( PHDs / HPHs ). |
| Score | Text |
|---|---|
| 0.9996 | Despite the identification of a conserved Leu - X - X - Leu - Ala - Pro motif, the molecular requirement of ProteinHIF - 1alpha for PHDs / HPHs binding remains elusive. |
| Score | Text |
|---|---|
| 0.9959 | Recently, we demonstrated that Leu - 574 of human ProteinHIF - 1alpha - - 10 residues downstream of Pro - 564 - - is essential for VHL recognition. |
| 0.9952 | Recently, we demonstrated that Leu - 574 of human HIF - 1alpha - - 10 residues downstream of Pro - 564 - - is essential for ProteinVHL recognition. |
| Score | Text |
|---|---|
| 0.9905 | We show here that the role of Leu - 574 is to recruit ProteinPHD2 / HPH2 for Pro - 564 hydroxylation. |
| 0.9351 | We show here that the role of Leu - 574 is to recruit PHD2 / HPH2 for EntityPro - 564 hydroxylation. |
| 0.6596 | We show here that the role of Leu - 574 is to recruit PHD2 / HPH2 for Pro - 564 Hydroxylationhydroxylation . |
| We show here that the role of Leu - 574 is to recruit PHD2 / HPH2 for Pro - 564 Catalysishydroxylation . | |
| Score | Text |
|---|---|
| 0.9870 | An antibody specific for hydroxylated Pro - 564 has been used to determine the hydroxylation status ; mutation or deletion of Leu - 574 results in a significant decrease in the ratio of the hydroxylated ProteinHIF - 1alpha to the total amount. |
| 0.9752 | An antibody specific for Hydroxylationhydroxylated Pro - 564 has been used to determine the hydroxylation status ; mutation or deletion of Leu - 574 results in a significant decrease in the ratio of the hydroxylated HIF - 1alpha to the total amount. |
| 0.9707 | An antibody specific for hydroxylated Pro - 564 has been used to determine the hydroxylation status ; mutation or deletion of Leu - 574 results in a significant decrease in the ratio of the Hydroxylationhydroxylated HIF - 1alpha to the total amount. |
| 0.9686 | An antibody specific for hydroxylated EntityPro - 564 has been used to determine the hydroxylation status ; mutation or deletion of Leu - 574 results in a significant decrease in the ratio of the hydroxylated HIF - 1alpha to the total amount. |
| 0.9620 | An antibody specific for hydroxylated Pro - 564 has been used to determine the Hydroxylationhydroxylation status ; mutation or deletion of Leu - 574 results in a significant decrease in the ratio of the hydroxylated HIF - 1alpha to the total amount. |
| Score | Text |
|---|---|
| 0.9767 | The nine - residue spacing between Pro - 564 and Leu - 574 is not obligatory for prolyl Hydroxylationhydroxylation . |
| 0.9677 | The nine - residue spacing between Pro - 564 and Leu - 574 is not obligatory for Entityprolyl hydroxylation. |
| Score | Text |
|---|---|
| 0.9998 | Furthermore, mutation of Leu - 574 disrupts the binding of ProteinPHD2 / HPH2 , a key prolyl hydroxylase for oxygen - dependent proteolysis of HIF - 1alpha. |
| 0.9965 | Furthermore, mutation of Leu - 574 disrupts the binding of PHD2 / HPH2, a key prolyl hydroxylase for oxygen - dependent proteolysis of ProteinHIF - 1alpha . |
| Score | Text |
|---|---|
| 0.9998 | Hence, our findings indicate that Leu - 574 is essential for recruiting ProteinPHD2 / HPH2 , thereby providing a molecular basis for modulating HIF - 1alpha activity. |
| 0.9995 | Hence, our findings indicate that Leu - 574 is essential for recruiting PHD2 / HPH2, thereby providing a molecular basis for modulating ProteinHIF - 1alpha activity. |
| Score | Text |
|---|---|
| 0.9990 | ProteinTransferrin microheterogeneity in fetal blood. |
| Score | Text |
|---|---|
| 0.9997 | OBJECTIVES : To investigate the distribution of microheterogeneous subfractions of Proteintransferrin in fetal blood and the influence of highly sialylated transferrins on fetal growth. |
| 0.9996 | OBJECTIVES : To investigate the distribution of microheterogeneous subfractions of transferrin in fetal blood and the influence of highly sialylated Proteintransferrins on fetal growth. |
| Score | Text |
|---|---|
| 0.9974 | STUDY METHOD : Serum Proteintransferrin concentrations were determined by a standard turbidimetric assay. |
| Score | Text |
|---|---|
| 0.9993 | Microheterogeneous Proteintransferrin subfractions were assessed by crossed immunoisoelectric focusing. |
| Score | Text |
|---|---|
| 0.9990 | RESULTS : In normal term infants, total serum transferrin concentrations and percent distribution of highly sialylated Proteintransferrins ( > or = 5 - sialo - transferrins ) were markedly lower ; the percent distributions of hyposialylated transferrins ( 0 - and 1 - sialo - transferrins ) were apparently higher than those in non - pregnant and pregnant women. |
| 0.9989 | RESULTS : In normal term infants, total serum Proteintransferrin concentrations and percent distribution of highly sialylated transferrins ( > or = 5 - sialo - transferrins ) were markedly lower ; the percent distributions of hyposialylated transferrins ( 0 - and 1 - sialo - transferrins ) were apparently higher than those in non - pregnant and pregnant women. |
| 0.9983 | RESULTS : In normal term infants, total serum transferrin concentrations and percent distribution of highly sialylated transferrins ( > or = 5 - sialo - transferrins ) were markedly lower ; the percent distributions of hyposialylated Proteintransferrins ( 0 - and 1 - sialo - transferrins ) were apparently higher than those in non - pregnant and pregnant women. |
| 0.9975 | RESULTS : In normal term infants, total serum transferrin concentrations and percent distribution of highly sialylated transferrins ( > or = Protein5 - sialo - transferrins ) were markedly lower ; the percent distributions of hyposialylated transferrins ( 0 - and 1 - sialo - transferrins ) were apparently higher than those in non - pregnant and pregnant women. |
| 0.9891 | RESULTS : In normal term infants, total serum transferrin concentrations and percent distribution of highly sialylated transferrins ( > or = 5 - sialo - transferrins ) were markedly lower ; the percent distributions of hyposialylated transferrins ( 0 - and Protein1 - sialo - transferrins ) were apparently higher than those in non - pregnant and pregnant women. |
| Score | Text |
|---|---|
| 0.9995 | There was no significant positive correlation between the serum concentrations of total Proteintransferrin or highly sialylated transferrins in infants'blood and birth weights ( r = 0. 187, p = 0. 582 ; r = 0. 374, p = 0. 257, respectively ). |
| 0.9993 | There was no significant positive correlation between the serum concentrations of total transferrin or highly sialylated Proteintransferrins in infants'blood and birth weights ( r = 0. 187, p = 0. 582 ; r = 0. 374, p = 0. 257, respectively ). |
| Score | Text |
|---|---|
| 0.9995 | CONCLUSION : The Proteintransferrin microheterogeneity pattern shifted towards reduced glycosylation and sialylation in addition to a decrease in total transferrin concentration in fetal blood compared to that of non - pregnant and pregnant women. |
| 0.9990 | CONCLUSION : The transferrin microheterogeneity pattern shifted towards reduced glycosylation and sialylation in addition to a decrease in total Proteintransferrin concentration in fetal blood compared to that of non - pregnant and pregnant women. |
| 0.9738 | CONCLUSION : The transferrin microheterogeneity pattern shifted towards reduced Glycosylationglycosylation and sialylation in addition to a decrease in total transferrin concentration in fetal blood compared to that of non - pregnant and pregnant women. |
| Score | Text |
|---|---|
| 0.9996 | The concentrations of serum total Proteintransferrin and the highly sialylated transferrins in fetal blood, if higher than a certain level, did not seem to have any influence on normal fetal growth. |
| 0.9993 | The concentrations of serum total transferrin and the highly sialylated Proteintransferrins in fetal blood, if higher than a certain level, did not seem to have any influence on normal fetal growth. |
| Score | Text |
|---|---|
| 0.9742 | Heterochromatin and Methylationtri - methylated lysine 20 of histone H4 in animals. |
| 0.9268 | Heterochromatin and tri - methylated lysine 20 of Proteinhistone H4 in animals. |
| 0.8498 | Heterochromatin and tri - methylated Entitylysine 20 of histone H4 in animals. |
| Score | Text |
|---|---|
| 0.9874 | MethylationTri - methylated lysine 20 on histone H4 ( Me ( 3 ) K20H4 ) is a marker of constitutive heterochromatin in murine interphase and metaphase cells. |
| 0.8946 | Tri - methylated Entitylysine 20 on histone H4 ( Me ( 3 ) K20H4 ) is a marker of constitutive heterochromatin in murine interphase and metaphase cells. |
| 0.8809 | Tri - methylated lysine 20 on Proteinhistone H4 ( Me ( 3 ) K20H4 ) is a marker of constitutive heterochromatin in murine interphase and metaphase cells. |
| 0.6483 | Tri - methylated lysine 20 on histone H4 Protein( Me ( 3 ) K20H4 ) is a marker of constitutive heterochromatin in murine interphase and metaphase cells. |
| 0.5268 | Tri - methylated Entitylysine 20 on histone H4 ( Me ( 3 ) K20H4 ) is a marker of constitutive heterochromatin in murine interphase and metaphase cells. |
| 0.5082 | Tri - methylated lysine 20 on Proteinhistone H4 ( Me ( 3 ) K20H4 ) is a marker of constitutive heterochromatin in murine interphase and metaphase cells. |
| Score | Text |
|---|---|
| 0.9916 | Heterochromatin marked by ProteinMe ( 3 ) K20H4 replicates late during S phase of the cell cycle. |
| Score | Text |
|---|---|
| 0.9752 | Serum starvation increases the number of cells that exhibit high levels of ProteinMe ( 3 ) K20H4 at constitutive heterochromatin. |
| Score | Text |
|---|---|
| 0.9932 | ProteinMe ( 3 ) K20H4 is also present at the centromeric heterochromatin of most meiotic chromosomes during spermatogenesis and at the pseudoautosomal region, as well as at some telomeres. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9655 | During murine embryogenesis the maternal pronucleus contains Me ( 3 ) K20H4 ; ProteinMe ( 3 ) K20H4 is absent from the paternal pronucleus. |
| 0.9477 | During murine embryogenesis the maternal pronucleus contains ProteinMe ( 3 ) K20H4 ; Me ( 3 ) K20H4 is absent from the paternal pronucleus. |
| 0.9399 | During murine embryogenesis the maternal pronucleus contains ProteinMe ( 3 ) K20H4 ; Me ( 3 ) K20H4 is absent from the paternal pronucleus. |
| Score | Text |
|---|---|
| 0.9936 | On Drosophila polytene chromosomes ProteinMe ( 3 ) K20H4 is present in a'punctate pattern'at many chromosomal bands, including the chromocenter. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9988 | We also present evidence that Me ( 3 ) K20H4 is dependent upon H3 - specific Suv ( 3 ) 9 histone methyltransferase activity, suggesting that there may be'epigenetic cross - talk'between histones H3 and ProteinH4 . |
| 0.9911 | We also present evidence that ProteinMe ( 3 ) K20H4 is dependent upon H3 - specific Suv ( 3 ) 9 histone methyltransferase activity, suggesting that there may be'epigenetic cross - talk'between histones H3 and H4. |
| 0.9697 | We also present evidence that Me ( 3 ) K20H4 is dependent upon H3 - specific Suv ( 3 ) 9 histone methyltransferase activity, suggesting that there may be'epigenetic cross - talk'between Proteinhistones H3 and H4. |
| 0.6694 | We also present evidence that Me ( 3 ) K20H4 is dependent upon ProteinH3 - specific Suv ( 3 ) 9 histone methyltransferase activity, suggesting that there may be'epigenetic cross - talk'between histones H3 and H4. |
| 0.6830 | We also present evidence that Me ( 3 ) K20H4 is dependent upon H3 - specific ProteinSuv ( 3 ) 9 histone methyltransferase activity, suggesting that there may be'epigenetic cross - talk'between histones H3 and H4. |
| 0.6558 | We also present evidence that Me ( 3 ) K20H4 is dependent upon H3 - specific Suv ( 3 ) 9 Proteinhistone methyltransferase activity, suggesting that there may be'epigenetic cross - talk'between histones H3 and H4. |
| Score | Text |
|---|---|
| 0.9991 | The Proteinhistone modification pattern of active genes revealed through genome - wide chromatin analysis of a higher eukaryote. |
| Score | Text |
|---|---|
| 0.9890 | The covalent modification of nucleosomal Proteinhistones has emerged as a major determinant of chromatin structure and gene activity. |
| Score | Text |
|---|---|
| 0.9949 | To understand the interplay between various Proteinhistone modifications, including acetylation and methylation, we performed a genome - wide chromatin structure analysis in a higher eukaryote. |
| 0.9871 | To understand the interplay between various histone modifications, including Acetylationacetylation and methylation, we performed a genome - wide chromatin structure analysis in a higher eukaryote. |
| 0.8893 | To understand the interplay between various histone modifications, including acetylation and Methylationmethylation , we performed a genome - wide chromatin structure analysis in a higher eukaryote. |
| Score | Text |
|---|---|
| 0.9949 | We found a binary pattern of Proteinhistone modifications among euchromatic genes, with active genes being hyperacetylated for H3 and H4 and hypermethylated at Lys 4 and Lys 79 of H3, and inactive genes being hypomethylated and deacetylated at the same residues. |
| 0.9866 | We found a binary pattern of histone modifications among euchromatic genes, with active genes being hyperacetylated for H3 and H4 and hypermethylated at Lys 4 and Lys 79 of ProteinH3 , and inactive genes being hypomethylated and deacetylated at the same residues. |
| 0.9506 | We found a binary pattern of histone modifications among euchromatic genes, with active genes being hyperacetylated for H3 and ProteinH4 and hypermethylated at Lys 4 and Lys 79 of H3, and inactive genes being hypomethylated and deacetylated at the same residues. |
| 0.9282 | We found a binary pattern of histone modifications among euchromatic genes, with active genes being hyperacetylated for ProteinH3 and H4 and hypermethylated at Lys 4 and Lys 79 of H3, and inactive genes being hypomethylated and deacetylated at the same residues. |
| 0.9132 | We found a binary pattern of histone modifications among euchromatic genes, with active genes being hyperacetylated for H3 and H4 and hypermethylated at Lys 4 and EntityLys 79 of H3, and inactive genes being hypomethylated and deacetylated at the same residues. |
| 0.8731 | We found a binary pattern of histone modifications among euchromatic genes, with active genes being hyperacetylated for H3 and H4 and hypermethylated at EntityLys 4 and Lys 79 of H3, and inactive genes being hypomethylated and deacetylated at the same residues. |
| 0.8616 | We found a binary pattern of histone modifications among euchromatic genes, with active genes being Acetylationhyperacetylated for H3 and H4 and hypermethylated at Lys 4 and Lys 79 of H3, and inactive genes being hypomethylated and deacetylated at the same residues. |
| 0.7554 | We found a binary pattern of histone modifications among euchromatic genes, with active genes being hyperacetylated for H3 and H4 and Methylationhypermethylated at Lys 4 and Lys 79 of H3, and inactive genes being hypomethylated and deacetylated at the same residues. |
| 0.6054 | We found a binary pattern of histone modifications among euchromatic genes, with active genes being hyperacetylated for H3 and H4 and hypermethylated at Lys 4 and Lys 79 of H3, and inactive genes being Methylationhypomethylated and deacetylated at the same residues. |
| 0.3837 | We found a binary pattern of histone modifications among euchromatic genes, with active genes being hyperacetylated for H3 and H4 and hypermethylated at Lys 4 and Lys 79 of H3, and inactive genes being hypomethylated and Deacetylationdeacetylated at the same residues. |
| 0.7354 | We found a binary pattern of histone modifications among euchromatic genes, with active genes being hyperacetylated for H3 and H4 and hypermethylated at Lys 4 and EntityLys 79 of H3, and inactive genes being hypomethylated and deacetylated at the same residues. |
| 0.6472 | We found a binary pattern of histone modifications among euchromatic genes, with active genes being hyperacetylated for H3 and H4 and hypermethylated at EntityLys 4 and Lys 79 of H3, and inactive genes being hypomethylated and deacetylated at the same residues. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9920 | Less frequent promoter DNA_methylationhypermethylation of DLC - 1 gene in primary breast cancers. |
| 0.9892 | Less frequent promoter hypermethylation of ProteinDLC - 1 gene in primary breast cancers. |
| 0.9601 | Less frequent Entitypromoter hypermethylation of DLC - 1 gene in primary breast cancers. |
| Score | Text |
|---|---|
| 0.9988 | Absence or low expression of ProteinDLC - 1 , a tumor suppressor gene, in breast cancers has been shown recently. |
| Score | Text |
|---|---|
| 0.9993 | LOH of 8p12 - p22, on which DLC - 1 is located, is frequent in breast cancers, but the correlation between low expression of ProteinDLC - 1 and LOH has not been confirmed. |
| 0.9977 | LOH of 8p12 - p22, on which ProteinDLC - 1 is located, is frequent in breast cancers, but the correlation between low expression of DLC - 1 and LOH has not been confirmed. |
| Score | Text |
|---|---|
| 0.9866 | To determine the implication of aberrant methylation, one of the most frequent mechanisms of silencing the tumor suppressor or cancer - related genes, we examined the DNA_methylationmethylation status of DLC - 1 promoter region in breast cancer cell lines and primary breast tumors. |
| 0.9374 | To determine the implication of aberrant methylation, one of the most frequent mechanisms of silencing the tumor suppressor or cancer - related genes, we examined the methylation status of ProteinDLC - 1 promoter region in breast cancer cell lines and primary breast tumors. |
| 0.9167 | To determine the implication of aberrant methylation, one of the most frequent mechanisms of silencing the tumor suppressor or cancer - related genes, we examined the methylation status of DLC - 1 Entitypromoter region in breast cancer cell lines and primary breast tumors. |
| 0.9389 | To determine the implication of aberrant methylation, one of the most frequent mechanisms of silencing the tumor suppressor or cancer - related genes, we examined the methylation status of DLC - 1 Entitypromoter region in breast cancer cell lines and primary breast tumors. |
| 0.8262 | To determine the implication of aberrant DNA_methylationmethylation , one of the most frequent mechanisms of silencing the tumor suppressor or cancer - related genes, we examined the methylation status of DLC - 1 promoter region in breast cancer cell lines and primary breast tumors. |
| 0.5645 | To determine the implication of aberrant methylation, one of the most frequent mechanisms of silencing the tumor suppressor or cancer - related genes, we examined the methylation status of DLC - 1 promoter Entityregion in breast cancer cell lines and primary breast tumors. |
| Score | Text |
|---|---|
| 0.9837 | The hypermethylation status was examined by MSP and 25 % of cell lines harbored a DNA_methylationmethylated allele. |
| Score | Text |
|---|---|
| 0.9996 | The gene silencing by methylation was also confirmed by the re - expression of ProteinDLC - 1 by the 5 - aza - 2'- deoxycytidine treatment in DLC - 1 hypermethylated cell line. |
| 0.9959 | The gene silencing by methylation was also confirmed by the re - expression of DLC - 1 by the 5 - aza - 2'- deoxycytidine treatment in ProteinDLC - 1 hypermethylated cell line. |
| 0.9005 | The gene silencing by methylation was also confirmed by the re - expression of DLC - 1 by the 5 - aza - 2'- deoxycytidine treatment in DLC - 1 DNA_methylationhypermethylated cell line. |
| 0.8026 | The gene silencing by DNA_methylationmethylation was also confirmed by the re - expression of DLC - 1 by the 5 - aza - 2'- deoxycytidine treatment in DLC - 1 hypermethylated cell line. |
| Score | Text |
|---|---|
| 0.9972 | But the methylation of ProteinDLC - 1 gene was less frequently shown in primary breast cancers ( 10 % ). |
| 0.9943 | But the DNA_methylationmethylation of DLC - 1 gene was less frequently shown in primary breast cancers ( 10 % ). |
| Score | Text |
|---|---|
| 0.9911 | These data suggest that hypermethylation is responsible for silencing of ProteinDLC - 1 gene in a limited portion of breast cancers. |
| 0.9896 | These data suggest that DNA_methylationhypermethylation is responsible for silencing of DLC - 1 gene in a limited portion of breast cancers. |
| Score | Text |
|---|---|
| 0.9962 | Glycosylation of the ProteinENV spike of primate immunodeficiency viruses and antibody neutralization. |
| 0.9626 | GlycosylationGlycosylation of the ENV spike of primate immunodeficiency viruses and antibody neutralization. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9999 | The logical target of protective antibody responses elicited by potential HIV vaccines should be the viral ProteinEnv spike on the surface of the virion. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9998 | This is thought to be a result of a combination of immunodominance of hypervariable regions of the ProteinEnv protein that can easily escape neutralization, antibody reactivity to gp160 " decoy " protein in cell surface debris or monomeric gp120, conformational constraints within the Env trimer that create unfavorable antibody binding conditions and extensive glycosylation of the exposed regions of Env within the trimer. |
| 0.9998 | This is thought to be a result of a combination of immunodominance of hypervariable regions of the Env protein that can easily escape neutralization, antibody reactivity to gp160 " decoy " protein in cell surface debris or monomeric gp120, conformational constraints within the ProteinEnv trimer that create unfavorable antibody binding conditions and extensive glycosylation of the exposed regions of Env within the trimer. |
| 0.9990 | This is thought to be a result of a combination of immunodominance of hypervariable regions of the Env protein that can easily escape neutralization, antibody reactivity to gp160 " decoy " protein in cell surface debris or monomeric gp120, conformational constraints within the Env trimer that create unfavorable antibody binding conditions and extensive glycosylation of the exposed regions of ProteinEnv within the trimer. |
| 0.9984 | This is thought to be a result of a combination of immunodominance of hypervariable regions of the Env protein that can easily escape neutralization, antibody reactivity to Proteingp160 " decoy " protein in cell surface debris or monomeric gp120, conformational constraints within the Env trimer that create unfavorable antibody binding conditions and extensive glycosylation of the exposed regions of Env within the trimer. |
| 0.9979 | This is thought to be a result of a combination of immunodominance of hypervariable regions of the Env protein that can easily escape neutralization, antibody reactivity to gp160 " decoy " protein in cell surface debris or monomeric Proteingp120 , conformational constraints within the Env trimer that create unfavorable antibody binding conditions and extensive glycosylation of the exposed regions of Env within the trimer. |
| 0.9382 | This is thought to be a result of a combination of immunodominance of hypervariable regions of the Env protein that can easily escape neutralization, antibody reactivity to gp160 " decoy " protein in cell surface debris or monomeric gp120, conformational constraints within the Env trimer that create unfavorable antibody binding conditions and extensive Glycosylationglycosylation of the exposed regions of Env within the trimer. |
| Score | Text |
|---|---|
| Score | Text |
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| 0.9996 | Part of the strategy toward development of an optimally immunogenic ProteinEnv spike will likely require modification of Env glycosylation. |
| 0.9977 | Part of the strategy toward development of an optimally immunogenic Env spike will likely require modification of ProteinEnv glycosylation. |
| 0.9750 | Part of the strategy toward development of an optimally immunogenic Env spike will likely require modification of Env Glycosylationglycosylation . |
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| 0.9094 | Comparison of methylation - specific polymerase chain reaction ( MSP ) with Proteinreverse transcriptase - polymerase chain reaction ( RT - PCR ) in peripheral blood of gastric cancer patients. |
| 0.7326 | Comparison of methylation - specific polymerase chain reaction ( MSP ) with reverse Proteintranscriptase - polymerase chain reaction ( RT - PCR ) in peripheral blood of gastric cancer patients. |
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| 0.9988 | This study was designed to compare carcinoembryonic antigen ( CEA ) - specific reverse transcriptase - polymerase chain reaction ( RT - PCR ) and methylation - specific polymerase chain reaction ( MSP ) for p16, ProteinE - cadherin , and retinoic acid receptor beta ( RARbeta ) genes using blood samples from gastric cancer patients. |
| 0.9987 | This study was designed to compare carcinoembryonic antigen ( CEA ) - specific reverse transcriptase - polymerase chain reaction ( RT - PCR ) and methylation - specific polymerase chain reaction ( MSP ) for Proteinp16 , E - cadherin, and retinoic acid receptor beta ( RARbeta ) genes using blood samples from gastric cancer patients. |
| 0.9615 | This study was designed to compare carcinoembryonic antigen ( CEA ) - specific reverse transcriptase - polymerase chain reaction ( RT - PCR ) and methylation - specific polymerase chain reaction ( MSP ) for p16, E - cadherin, and retinoic acid receptor beta Protein( RARbeta ) genes using blood samples from gastric cancer patients. |
| 0.9401 | This study was designed to compare carcinoembryonic antigen ( CEA ) - specific reverse transcriptase - polymerase chain reaction ( RT - PCR ) and methylation - specific polymerase chain reaction ( MSP ) for p16, E - cadherin, and Proteinretinoic acid receptor beta ( RARbeta ) genes using blood samples from gastric cancer patients. |
| 0.9394 | This study was designed to compare carcinoembryonic antigen ( CEA ) - specific Proteinreverse transcriptase - polymerase chain reaction ( RT - PCR ) and methylation - specific polymerase chain reaction ( MSP ) for p16, E - cadherin, and retinoic acid receptor beta ( RARbeta ) genes using blood samples from gastric cancer patients. |
| 0.8514 | This study was designed to compare carcinoembryonic antigen ( CEA ) - specific reverse Proteintranscriptase - polymerase chain reaction ( RT - PCR ) and methylation - specific polymerase chain reaction ( MSP ) for p16, E - cadherin, and retinoic acid receptor beta ( RARbeta ) genes using blood samples from gastric cancer patients. |
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| 0.9973 | The MSP assay detected hypermethylation of Proteinp16 in 9 patients ( 22 % ), E - cadherin in 9 patients ( 22 % ), and RARbeta in 6 patients ( 15 % ). |
| 0.9958 | The MSP assay detected hypermethylation of p16 in 9 patients ( 22 % ), E - cadherin in 9 patients ( 22 % ), and ProteinRARbeta in 6 patients ( 15 % ). |
| 0.9950 | The MSP assay detected hypermethylation of p16 in 9 patients ( 22 % ), ProteinE - cadherin in 9 patients ( 22 % ), and RARbeta in 6 patients ( 15 % ). |
| 0.9851 | The MSP assay detected DNA_methylationhypermethylation of p16 in 9 patients ( 22 % ), E - cadherin in 9 patients ( 22 % ), and RARbeta in 6 patients ( 15 % ). |
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| 0.4971 | Altogether, 18 patients ( 44 % ) showed DNA_methylationhypermethylation . |
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| 0.9985 | Superoxide dismutase and Proteincatalase are required to detect (. - ) NO from both coupled and uncoupled neuronal no synthase. |
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| 0.9846 | Despite numerous approaches to measuring nitric oxide ( (. - ) NO ) formation from purified NO synthase Protein( NOS ) , it is still not clear whether (. - ) NO is a direct or indirect product of the NO synthase reaction. |
| 0.9135 | Despite numerous approaches to measuring nitric oxide ( (. - ) NO ) formation from purified ProteinNO synthase ( NOS ), it is still not clear whether (. - ) NO is a direct or indirect product of the NO synthase reaction. |
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| 0.9993 | In conclusion, standard Clark - type ( ) NO electrodes are cross - sensitive to H ( 2 ) O ( 2 ) and therefore both SOD and Proteincatalase are absolutely required to specifically detect (. - ) NO from NOS. |
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| 0.9997 | We also found that the transcription of a pathway - specific regulator, Proteingra - ORF9 , was activated by exogenous SAM treatment. |
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| 0.9701 | We show that the glucosyltransferase domain of lethal toxin from Clostridium sordellii Protein( LT ( cyt ) ; amino acids 1 - 546 ), which is released into the cytosol during cell infection, binds preferentially to liposomes containing phosphatidylserine as compared with other anionic lipids. |
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| 0.9985 | The binding of ProteinLT ( cyt ) to phosphatidylserine increases by two orders of magnitude the rate of glucosylation of liposome - bound geranyl - geranylated Rac - GDP. |
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| 0.9940 | Limited proteolysis and deletion studies show that the binding site for phosphatidylserine lies within the first 18 N - terminal residues of ProteinLT ( cyt ) . |
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| 0.9985 | Deletion of these residues abolishes the effect of phosphatidylserine on the activity of ProteinLT ( cyt ) on liposome - bound geranyl - geranylated Rac - GDP and prevents the morphological effects induced by LT ( cyt ) microinjection into various cells, but it does not affect the intrinsic activity of LT ( cyt ) on non - geranyl - geranylated Rac - GDP in solution. |
| 0.9978 | Deletion of these residues abolishes the effect of phosphatidylserine on the activity of LT ( cyt ) on liposome - bound geranyl - geranylated Rac - GDP and prevents the morphological effects induced by ProteinLT ( cyt ) microinjection into various cells, but it does not affect the intrinsic activity of LT ( cyt ) on non - geranyl - geranylated Rac - GDP in solution. |
| 0.9972 | Deletion of these residues abolishes the effect of phosphatidylserine on the activity of LT ( cyt ) on liposome - bound geranyl - geranylated Rac - GDP and prevents the morphological effects induced by LT ( cyt ) microinjection into various cells, but it does not affect the intrinsic activity of ProteinLT ( cyt ) on non - geranyl - geranylated Rac - GDP in solution. |
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| 0.9984 | We conclude that the avidity of ProteinLT ( cyt ) for phosphatidylserine facilitates its targeting to the cytosolic leaflet of cell membranes and, notably, the plasma membrane, where this anionic lipid is abundant and where several targets of lethal toxin reside. |
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| 0.9663 | Site - specific substitutions of arginine for lysine in the thermostable D - xylose isomerase Protein( XI ) from Actinoplanes missouriensis are shown to impart significant heat stability enhancement in the presence of sugar substrates most probably by interfering with nonenzymatic glycation. |
| 0.9347 | Site - specific substitutions of arginine for lysine in the thermostable ProteinD - xylose isomerase ( XI ) from Actinoplanes missouriensis are shown to impart significant heat stability enhancement in the presence of sugar substrates most probably by interfering with nonenzymatic glycation. |
| 0.5951 | Site - specific substitutions of arginine for lysine in the thermostable ProteinD - xylose isomerase ( XI ) from Actinoplanes missouriensis are shown to impart significant heat stability enhancement in the presence of sugar substrates most probably by interfering with nonenzymatic glycation. |
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| 0.9819 | This rather conservative substitution is moreover shown to improve thermostability in two other structurally unrelated proteins, human copper, zinc - superoxide dismutase ( CuZnSOD ) and D - glyceraldehyde - 3 - phosphate dehydrogenase Protein( GAPDH ) from Bacillus subtilis. |
| 0.9721 | This rather conservative substitution is moreover shown to improve thermostability in two other structurally unrelated proteins, human copper, zinc - superoxide dismutase Protein( CuZnSOD ) and D - glyceraldehyde - 3 - phosphate dehydrogenase ( GAPDH ) from Bacillus subtilis. |
| 0.9103 | This rather conservative substitution is moreover shown to improve thermostability in two other structurally unrelated proteins, human copper, zinc - superoxide dismutase ( CuZnSOD ) and ProteinD - glyceraldehyde - 3 - phosphate dehydrogenase ( GAPDH ) from Bacillus subtilis. |
| 0.8498 | This rather conservative substitution is moreover shown to improve thermostability in two other structurally unrelated proteins, human Proteincopper, zinc - superoxide dismutase ( CuZnSOD ) and D - glyceraldehyde - 3 - phosphate dehydrogenase ( GAPDH ) from Bacillus subtilis. |
| 0.8003 | This rather conservative substitution is moreover shown to improve thermostability in two other structurally unrelated proteins, human copper, Proteinzinc - superoxide dismutase ( CuZnSOD ) and D - glyceraldehyde - 3 - phosphate dehydrogenase ( GAPDH ) from Bacillus subtilis. |
| 0.7742 | This rather conservative substitution is moreover shown to improve thermostability in two other structurally unrelated proteins, human copper Protein, zinc - superoxide dismutase ( CuZnSOD ) and D - glyceraldehyde - 3 - phosphate dehydrogenase ( GAPDH ) from Bacillus subtilis. |
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|---|---|
| 0.9960 | The stabilizing effect of Lys - - - - Arg substitutions is rationalized on the basis of a detailed analysis of the crystal structures of wild - type ProteinXI and of engineered variants with Lys - - - - Arg substitution at four distinct locations, residues 253, 309, 319, and 323. |
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|---|---|
| 0.9974 | Molecular model building analysis of the structures of wild - type and mutant CuZnSOD ( K9R ) and ProteinGAPDH ( G281K and G281R ) is used to explain the observed stability enhancement in these proteins. |
| 0.9869 | Molecular model building analysis of the structures of wild - type and mutant ProteinCuZnSOD ( K9R ) and GAPDH ( G281K and G281R ) is used to explain the observed stability enhancement in these proteins. |
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|---|---|
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| 0.9929 | Human SWI / SNF - associated PRMT5 methylates histone H3 arginine 8 and negatively regulates expression of ST7 and ProteinNM23 tumor suppressor genes. |
| 0.9891 | Human SWI / SNF - associated ProteinPRMT5 methylates histone H3 arginine 8 and negatively regulates expression of ST7 and NM23 tumor suppressor genes. |
| 0.9872 | Human SWI / SNF - associated PRMT5 methylates histone H3 arginine 8 and negatively regulates expression of ProteinST7 and NM23 tumor suppressor genes. |
| 0.5813 | Human SWI / SNF - associated PRMT5 methylates Proteinhistone H3 arginine 8 and negatively regulates expression of ST7 and NM23 tumor suppressor genes. |
| 0.5519 | Human SWI / SNF - associated PRMT5 methylates histone H3 Entityarginine 8 and negatively regulates expression of ST7 and NM23 tumor suppressor genes. |
| 0.5334 | Human SWI / SNF - associated PRMT5 Methylationmethylates histone H3 arginine 8 and negatively regulates expression of ST7 and NM23 tumor suppressor genes. |
| Human SWI / SNF - associated PRMT5 Catalysismethylates histone H3 arginine 8 and negatively regulates expression of ST7 and NM23 tumor suppressor genes. | |
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| 0.9994 | We have recently shown that ProteinPRMT5 can interact with flag - tagged BRG1 - and hBRM - based hSWI / SNF chromatin remodelers and that both complexes can specifically methylate histones H3 and H4. |
| 0.9992 | We have recently shown that PRMT5 can interact with flag - tagged ProteinBRG1 - and hBRM - based hSWI / SNF chromatin remodelers and that both complexes can specifically methylate histones H3 and H4. |
| 0.9968 | We have recently shown that PRMT5 can interact with flag - tagged BRG1 - and ProteinhBRM - based hSWI / SNF chromatin remodelers and that both complexes can specifically methylate histones H3 and H4. |
| 0.9908 | We have recently shown that PRMT5 can interact with flag - tagged BRG1 - and hBRM - based hSWI / SNF chromatin remodelers and that both complexes can specifically methylate histones H3 and ProteinH4 . |
| 0.9304 | We have recently shown that PRMT5 can interact with flag - tagged BRG1 - and hBRM - based hSWI / SNF chromatin remodelers and that both complexes can specifically methylate Proteinhistones H3 and H4. |
| 0.8629 | We have recently shown that PRMT5 can interact with flag - tagged BRG1 - and hBRM - based hSWI / SNF chromatin remodelers and that both complexes can specifically Methylationmethylate histones H3 and H4. |
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|---|---|
| 0.9991 | Here we report that PRMT5 can be found in association with endogenous hSWI / SNF complexes, which can methylate H3 and H4 N - terminal tails, and show that H3 arginine 8 and H4 arginine 3 are preferred sites of methylation by recombinant and hSWI / SNF - associated ProteinPRMT5 . |
| 0.9989 | Here we report that ProteinPRMT5 can be found in association with endogenous hSWI / SNF complexes, which can methylate H3 and H4 N - terminal tails, and show that H3 arginine 8 and H4 arginine 3 are preferred sites of methylation by recombinant and hSWI / SNF - associated PRMT5. |
| 0.9927 | Here we report that PRMT5 can be found in association with endogenous hSWI / SNF complexes, which can methylate H3 and ProteinH4 N - terminal tails, and show that H3 arginine 8 and H4 arginine 3 are preferred sites of methylation by recombinant and hSWI / SNF - associated PRMT5. |
| 0.9897 | Here we report that PRMT5 can be found in association with endogenous hSWI / SNF complexes, which can methylate ProteinH3 and H4 N - terminal tails, and show that H3 arginine 8 and H4 arginine 3 are preferred sites of methylation by recombinant and hSWI / SNF - associated PRMT5. |
| 0.9599 | Here we report that PRMT5 can be found in association with endogenous hSWI / SNF complexes, which can methylate H3 and H4 N - terminal tails, and show that ProteinH3 arginine 8 and H4 arginine 3 are preferred sites of methylation by recombinant and hSWI / SNF - associated PRMT5. |
| 0.9479 | Here we report that PRMT5 can be found in association with endogenous hSWI / SNF complexes, which can methylate H3 and H4 N - terminal tails, and show that H3 arginine 8 and ProteinH4 arginine 3 are preferred sites of methylation by recombinant and hSWI / SNF - associated PRMT5. |
| 0.9199 | Here we report that PRMT5 can be found in association with endogenous hSWI / SNF complexes, which can methylate H3 and H4 N - terminal tails, and show that H3 Entityarginine 8 and H4 arginine 3 are preferred sites of methylation by recombinant and hSWI / SNF - associated PRMT5. |
| 0.8236 | Here we report that PRMT5 can be found in association with endogenous hSWI / SNF complexes, which can methylate H3 and H4 N - terminal tails, and show that H3 arginine 8 and H4 Entityarginine 3 are preferred sites of methylation by recombinant and hSWI / SNF - associated PRMT5. |
| 0.6727 | Here we report that PRMT5 can be found in association with endogenous hSWI / SNF complexes, which can methylate H3 and H4 N - terminal tails, and show that H3 arginine 8 and H4 arginine 3 are preferred sites of Methylationmethylation by recombinant and hSWI / SNF - associated PRMT5. |
| 0.6351 | Here we report that PRMT5 can be found in association with endogenous hSWI / SNF complexes, which can methylate H3 and H4 N - terminal tails, and show that H3 Entityarginine 8 and H4 arginine 3 are preferred sites of methylation by recombinant and hSWI / SNF - associated PRMT5. |
| 0.5712 | Here we report that PRMT5 can be found in association with endogenous hSWI / SNF complexes, which can Catalysismethylate H3 and H4 N - terminal tails, and show that H3 arginine 8 and H4 arginine 3 are preferred sites of methylation by recombinant and hSWI / SNF - associated PRMT5. |
| Here we report that PRMT5 can be found in association with endogenous hSWI / SNF complexes, which can methylate H3 and H4 N - terminal tails, and show that H3 arginine 8 and H4 arginine 3 are preferred sites of Catalysismethylation by recombinant and hSWI / SNF - associated PRMT5. | |
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| 0.9985 | To elucidate the role played by ProteinPRMT5 in gene regulation, we have established a PRMT5 antisense cell line and determined by microarray analysis that more genes are derepressed when PRMT5 levels are reduced. |
| 0.9969 | To elucidate the role played by PRMT5 in gene regulation, we have established a ProteinPRMT5 antisense cell line and determined by microarray analysis that more genes are derepressed when PRMT5 levels are reduced. |
| 0.9962 | To elucidate the role played by PRMT5 in gene regulation, we have established a PRMT5 antisense cell line and determined by microarray analysis that more genes are derepressed when ProteinPRMT5 levels are reduced. |
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|---|---|
| 0.9962 | Among the affected genes, we show that suppressor of tumorigenicity 7 ( ST7 ) and nonmetastatic 23 ( NM23 ) are direct targets of PRMT5 - containing BRG1 and ProteinhBRM complexes. |
| 0.9935 | Among the affected genes, we show that suppressor of tumorigenicity 7 ( ST7 ) and nonmetastatic 23 ( NM23 ) are direct targets of PRMT5 - containing ProteinBRG1 and hBRM complexes. |
| 0.9745 | Among the affected genes, we show that suppressor of tumorigenicity 7 ( ST7 ) and nonmetastatic 23 Protein( NM23 ) are direct targets of PRMT5 - containing BRG1 and hBRM complexes. |
| 0.9604 | Among the affected genes, we show that suppressor of tumorigenicity 7 ( ST7 ) and nonmetastatic 23 ( NM23 ) are direct targets of ProteinPRMT5 - containing BRG1 and hBRM complexes. |
| 0.9591 | Among the affected genes, we show that suppressor of tumorigenicity 7 Protein( ST7 ) and nonmetastatic 23 ( NM23 ) are direct targets of PRMT5 - containing BRG1 and hBRM complexes. |
| 0.9141 | Among the affected genes, we show that suppressor of tumorigenicity 7 ( ST7 ) and Proteinnonmetastatic 23 ( NM23 ) are direct targets of PRMT5 - containing BRG1 and hBRM complexes. |
| 0.7518 | Among the affected genes, we show that Proteinsuppressor of tumorigenicity 7 ( ST7 ) and nonmetastatic 23 ( NM23 ) are direct targets of PRMT5 - containing BRG1 and hBRM complexes. |
| 0.9664 | Among the affected genes, we show that suppressor of tumorigenicity 7 ( ST7 ) and nonmetastatic 23 ( NM23 ) are direct targets of ProteinPRMT5 - containing BRG1 and hBRM complexes. |
| 0.5466 | Among the affected genes, we show that suppressor of Proteintumorigenicity 7 ( ST7 ) and nonmetastatic 23 ( NM23 ) are direct targets of PRMT5 - containing BRG1 and hBRM complexes. |
| 0.5392 | Among the affected genes, we show that suppressor Proteinof tumorigenicity 7 ( ST7 ) and nonmetastatic 23 ( NM23 ) are direct targets of PRMT5 - containing BRG1 and hBRM complexes. |
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|---|---|
| 0.9998 | Furthermore, we demonstrate that expression of ST7 and NM23 is reduced in a cell line that overexpresses ProteinPRMT5 and that this decrease in expression correlates with H3R8 methylation, H3K9 deacetylation, and increased transformation of NIH 3T3 cells. |
| 0.9988 | Furthermore, we demonstrate that expression of ProteinST7 and NM23 is reduced in a cell line that overexpresses PRMT5 and that this decrease in expression correlates with H3R8 methylation, H3K9 deacetylation, and increased transformation of NIH 3T3 cells. |
| 0.9984 | Furthermore, we demonstrate that expression of ST7 and ProteinNM23 is reduced in a cell line that overexpresses PRMT5 and that this decrease in expression correlates with H3R8 methylation, H3K9 deacetylation, and increased transformation of NIH 3T3 cells. |
| 0.7305 | Furthermore, we demonstrate that expression of ST7 and NM23 is reduced in a cell line that overexpresses PRMT5 and that this decrease in expression correlates with H3R8 Methylationmethylation , H3K9 deacetylation, and increased transformation of NIH 3T3 cells. |
| 0.6449 | Furthermore, we demonstrate that expression of ST7 and NM23 is reduced in a cell line that overexpresses PRMT5 and that this decrease in expression correlates with H3R8 methylation, EntityH3K9 deacetylation, and increased transformation of NIH 3T3 cells. |
| 0.5277 | Furthermore, we demonstrate that expression of ST7 and NM23 is reduced in a cell line that overexpresses PRMT5 and that this decrease in expression correlates with H3R8 methylation, H3K9 Deacetylationdeacetylation , and increased transformation of NIH 3T3 cells. |
| 0.5087 | Furthermore, we demonstrate that expression of ST7 and NM23 is reduced in a cell line that overexpresses PRMT5 and that this decrease in expression correlates with EntityH3R8 methylation, H3K9 deacetylation, and increased transformation of NIH 3T3 cells. |
| Furthermore, we demonstrate that expression of ST7 and NM23 is reduced in a cell line that overexpresses PRMT5 and that this decrease in expression correlates with ProteinH3R8 methylation, H3K9 deacetylation, and increased transformation of NIH 3T3 cells. | |
| Furthermore, we demonstrate that expression of ST7 and NM23 is reduced in a cell line that overexpresses PRMT5 and that this decrease in expression correlates with H3R8 methylation, ProteinH3K9 deacetylation, and increased transformation of NIH 3T3 cells. | |
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|---|---|
| 0.9970 | These findings suggest that the ProteinBRG1 - and hBRM - associated PRMT5 regulates cell growth and proliferation by controlling expression of genes involved in tumor suppression. |
| 0.9871 | These findings suggest that the BRG1 - and ProteinhBRM - associated PRMT5 regulates cell growth and proliferation by controlling expression of genes involved in tumor suppression. |
| 0.6126 | These findings suggest that the BRG1 - and hBRM - associated ProteinPRMT5 regulates cell growth and proliferation by controlling expression of genes involved in tumor suppression. |
| 0.8841 | These findings suggest that the BRG1 - and ProteinhBRM - associated PRMT5 regulates cell growth and proliferation by controlling expression of genes involved in tumor suppression. |
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| 0.9999 | In the current study, we examined the radiation - induced changes in expression of maintenance ProteinDNMT1 , and de novo methyltransferases DNMT3a and DNMT3b in spleen and liver of irradiated animals. |
| 0.9998 | In the current study, we examined the radiation - induced changes in expression of maintenance DNMT1, and de novo methyltransferases ProteinDNMT3a and DNMT3b in spleen and liver of irradiated animals. |
| 0.9998 | In the current study, we examined the radiation - induced changes in expression of maintenance DNMT1, and de novo methyltransferases DNMT3a and ProteinDNMT3b in spleen and liver of irradiated animals. |
| Score | Text |
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| 0.9998 | We present the data on tissue - specificity in radiation - induced expression of DNA methyltransferases, and prove that changes in the expression of de novo methyltransferases DNMT3a and ProteinDNMT3b are the most important in radiation - induced DNA methylation alterations. |
| 0.9998 | We present the data on tissue - specificity in radiation - induced expression of DNA methyltransferases, and prove that changes in the expression of de novo methyltransferases ProteinDNMT3a and DNMT3b are the most important in radiation - induced DNA methylation alterations. |
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| 0.9290 | To isolate useful microbial enzymes from uncultured soil microorganisms, a metagenome was isolated from soil samples, and a metagenomic library was constructed by using the ProteinpUC19 vector. |
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| 0.9974 | The putative amylase gene Protein( amyM ) was overexpressed and purified for characterization. |
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| 0.9989 | Optimal conditions for the enzyme activity of the ProteinAmyM protein were 42 degrees C and pH 9. 0 ; Ca2 + stabilized the activity. |
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| 0.9979 | The hydrolysis and transglycosylation properties of ProteinAmyM suggest that it has novel characteristics and can be regarded as an intermediate type of maltogenic amylase, alpha - amylase, and 4 - alpha - glucanotransferase. |
| 0.9341 | The hydrolysis and transglycosylation properties of AmyM suggest that it has novel characteristics and can be regarded as an intermediate type of maltogenic amylase, alpha - amylase, and Protein4 - alpha - glucanotransferase . |
| 0.4699 | The hydrolysis and Glycosylationtransglycosylation properties of AmyM suggest that it has novel characteristics and can be regarded as an intermediate type of maltogenic amylase, alpha - amylase, and 4 - alpha - glucanotransferase. |
| Score | Text |
|---|---|
| 0.8859 | Protein4 - Hydroxyphenylpyruvate dioxygenase . |
| Score | Text |
|---|---|
| 0.9759 | 4 - Hydroxyphenylpyruvate dioxygenase Protein( HPPD ) is an Fe ( II ) - dependent, non - heme oxygenase that catalyzes the conversion of 4 - hydroxyphenylpyruvate to homogentisate. |
| 0.8469 | Protein4 - Hydroxyphenylpyruvate dioxygenase ( HPPD ) is an Fe ( II ) - dependent, non - heme oxygenase that catalyzes the conversion of 4 - hydroxyphenylpyruvate to homogentisate. |
| Score | Text |
|---|---|
| Score | Text |
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| 0.9989 | ProteinHPPD is a member of the alpha - keto acid dependent oxygenases that typically require an alpha - keto acid ( almost exclusively alpha - ketoglutarate ) and molecular oxygen to either oxygenate or oxidize a third molecule. |
| Score | Text |
|---|---|
| 0.9988 | As an exception in this class of enzymes ProteinHPPD has only two substrates, does not use alpha - ketoglutarate, and incorporates both atoms of dioxygen into the aromatic product, homogentisate. |
| Score | Text |
|---|---|
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| 0.9997 | The transformation catalyzed by ProteinHPPD has both agricultural and therapeutic significance. |
| Score | Text |
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| 0.9989 | ProteinHPPD catalyzes the second step in the pathway for the catabolism of tyrosine, that is common to essentially all aerobic forms of life. |
| Score | Text |
|---|---|
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| 0.9989 | Naturally occurring multi - ketone molecules act as allelopathic agents by inhibiting ProteinHPPD and preventing the production of homogentisate and hence required redox cofactors. |
| Score | Text |
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| 0.9983 | Interestingly, ProteinHPPD inhibitor / herbicide molecules act also as therapeutic agents for a number of debilitating and lethal inborn defects in tyrosine catabolism by preventing the accumulation of toxic metabolites. |
| Score | Text |
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| 0.9881 | Distinct dynamics and distribution of Proteinhistone methyl - lysine derivatives in mouse development. |
| Score | Text |
|---|---|
| 0.9729 | Histone methylation acts as an epigenetic regulator of chromatin activity through the modification of arginine and lysine residues on histones H3 and ProteinH4 . |
| 0.9491 | Histone methylation acts as an epigenetic regulator of chromatin activity through the modification of arginine and lysine residues on Proteinhistones H3 and H4. |
| 0.9373 | Histone Methylationmethylation acts as an epigenetic regulator of chromatin activity through the modification of arginine and lysine residues on histones H3 and H4. |
| 0.9284 | ProteinHistone methylation acts as an epigenetic regulator of chromatin activity through the modification of arginine and lysine residues on histones H3 and H4. |
| 0.9095 | Histone methylation acts as an epigenetic regulator of chromatin activity through the modification of Entityarginine and lysine residues on histones H3 and H4. |
| 0.8980 | Histone methylation acts as an epigenetic regulator of chromatin activity through the modification of arginine and Entitylysine residues on histones H3 and H4. |
| 0.7104 | Histone methylation acts as an epigenetic regulator of chromatin activity through the modification of arginine and Entitylysine residues on histones H3 and H4. |
| 0.5154 | Histone methylation acts as an epigenetic regulator of chromatin activity through the modification of arginine and lysine residues on Proteinhistones H3 and H4. |
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| 0.9925 | To examine the potential developmental roles of these modifications, we determined the global patterns of lysine methylation involving K9 on histone H3 and EntityK20 on histone H4 in midgestation mouse embryos. |
| 0.9920 | To examine the potential developmental roles of these modifications, we determined the global patterns of lysine methylation involving EntityK9 on histone H3 and K20 on histone H4 in midgestation mouse embryos. |
| 0.9461 | To examine the potential developmental roles of these modifications, we determined the global patterns of lysine methylation involving K9 on Proteinhistone H3 and K20 on histone H4 in midgestation mouse embryos. |
| 0.9343 | To examine the potential developmental roles of these modifications, we determined the global patterns of lysine methylation involving K9 on histone H3 and K20 on Proteinhistone H4 in midgestation mouse embryos. |
| 0.9261 | To examine the potential developmental roles of these modifications, we determined the global patterns of lysine Methylationmethylation involving K9 on histone H3 and K20 on histone H4 in midgestation mouse embryos. |
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|---|---|
| Score | Text |
|---|---|
| 0.9743 | Interestingly, three of these modifications, histone H3 trimethyl EntityK9 , histone H4 monomethyl K20, and histone H4 trimethyl K20 exhibited marked differences in their distribution within the neuroepithelium. |
| 0.9684 | Interestingly, three of these modifications, histone H3 trimethyl K9, histone H4 monomethyl K20, and histone H4 trimethyl EntityK20 exhibited marked differences in their distribution within the neuroepithelium. |
| 0.9539 | Interestingly, three of these modifications, histone H3 trimethyl K9, histone H4 monomethyl EntityK20 , and histone H4 trimethyl K20 exhibited marked differences in their distribution within the neuroepithelium. |
| 0.9449 | Interestingly, three of these modifications, Proteinhistone H3 trimethyl K9, histone H4 monomethyl K20, and histone H4 trimethyl K20 exhibited marked differences in their distribution within the neuroepithelium. |
| 0.9394 | Interestingly, three of these modifications, histone H3 trimethyl K9, Proteinhistone H4 monomethyl K20, and histone H4 trimethyl K20 exhibited marked differences in their distribution within the neuroepithelium. |
| 0.9185 | Interestingly, three of these modifications, histone H3 trimethyl K9, histone H4 monomethyl K20, and Proteinhistone H4 trimethyl K20 exhibited marked differences in their distribution within the neuroepithelium. |
| 0.8652 | Interestingly, three of these Methylationmodifications , histone H3 trimethyl K9, histone H4 monomethyl K20, and histone H4 trimethyl K20 exhibited marked differences in their distribution within the neuroepithelium. |
| Score | Text |
|---|---|
| 0.9887 | Specifically, both histone H3 trimethyl K9 and ProteinH4 monomethyl K20 were elevated in proliferating cells of the neural tube, which in the case of the K9 modification was limited to mitotic cells on the luminal surface. |
| 0.9757 | Specifically, both histone H3 trimethyl K9 and H4 monomethyl K20 were elevated in proliferating cells of the neural tube, which in the case of the EntityK9 modification was limited to mitotic cells on the luminal surface. |
| 0.9641 | Specifically, both histone H3 trimethyl K9 and H4 monomethyl K20 were elevated in proliferating cells of the neural tube, which in the case of the K9 Methylationmodification was limited to mitotic cells on the luminal surface. |
| 0.9408 | Specifically, both Proteinhistone H3 trimethyl K9 and H4 monomethyl K20 were elevated in proliferating cells of the neural tube, which in the case of the K9 modification was limited to mitotic cells on the luminal surface. |
| 0.9344 | Specifically, both histone H3 trimethyl EntityK9 and H4 monomethyl K20 were elevated in proliferating cells of the neural tube, which in the case of the K9 modification was limited to mitotic cells on the luminal surface. |
| 0.8709 | Specifically, both histone H3 trimethyl K9 and H4 monomethyl EntityK20 were elevated in proliferating cells of the neural tube, which in the case of the K9 modification was limited to mitotic cells on the luminal surface. |
| Score | Text |
|---|---|
| 0.9584 | In contrast, Proteinhistone H4 trimethyl K20 was progressively lost from these medial regions and became enriched in differentiating neurons in the ventrolateral neural tube. |
| Score | Text |
|---|---|
| 0.9813 | The inverse relationship of histone H4 EntityK20 methyl derivatives is even more striking during skeletal and cardiac myogenesis where the accumulation of the trimethyl modification in pericentromeric heterochromatin suggests a role in gene silencing in postmitotic muscle cells. |
| 0.9358 | The inverse relationship of Proteinhistone H4 K20 methyl derivatives is even more striking during skeletal and cardiac myogenesis where the accumulation of the trimethyl modification in pericentromeric heterochromatin suggests a role in gene silencing in postmitotic muscle cells. |
| 0.9302 | The inverse relationship of histone H4 K20 methyl derivatives is even more striking during skeletal and cardiac myogenesis where the accumulation of the Methylationtrimethyl modification in pericentromeric heterochromatin suggests a role in gene silencing in postmitotic muscle cells. |
| 0.9676 | The inverse relationship of histone H4 K20 methyl derivatives is even more striking during skeletal and cardiac myogenesis where the accumulation of the Methylationtrimethyl modification in pericentromeric heterochromatin suggests a role in gene silencing in postmitotic muscle cells. |
| 0.7513 | The inverse relationship of histone H4 K20 Methylationmethyl derivatives is even more striking during skeletal and cardiac myogenesis where the accumulation of the trimethyl modification in pericentromeric heterochromatin suggests a role in gene silencing in postmitotic muscle cells. |
| 0.7046 | The inverse relationship of histone H4 K20 methyl derivatives is even more striking during skeletal and cardiac myogenesis where the accumulation of the trimethyl Methylationmodification in pericentromeric heterochromatin suggests a role in gene silencing in postmitotic muscle cells. |
| Score | Text |
|---|---|
| 0.9796 | Importantly, our results establish that histone lysine Methylationmethylation occurs in a highly dynamic manner that is consistent with their function in an epigenetic program for cell division and differentiation. |
| 0.9606 | Importantly, our results establish that histone Entitylysine methylation occurs in a highly dynamic manner that is consistent with their function in an epigenetic program for cell division and differentiation. |
| 0.9308 | Importantly, our results establish that Proteinhistone lysine methylation occurs in a highly dynamic manner that is consistent with their function in an epigenetic program for cell division and differentiation. |
| Score | Text |
|---|---|
| 0.9997 | Decreased expression of lysyl hydroxylase 2 ( LH2 ) in skin fibroblasts from three Ehlers - Danlos patients does not result from mutations in either the coding or proximal promoter region of the ProteinLH2 gene. |
| 0.9692 | Decreased expression of lysyl hydroxylase 2 Protein( LH2 ) in skin fibroblasts from three Ehlers - Danlos patients does not result from mutations in either the coding or proximal promoter region of the LH2 gene. |
| 0.8437 | Decreased expression of Proteinlysyl hydroxylase 2 ( LH2 ) in skin fibroblasts from three Ehlers - Danlos patients does not result from mutations in either the coding or proximal promoter region of the LH2 gene. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9967 | These patients have significantly decreased levels of lysyl hydroxylase ( LH ) activity, due to mutations in the ProteinLH1 gene. |
| Score | Text |
|---|---|
| 0.6730 | LH Hydroxylationhydroxylates specific lysine residues in the collagen molecule that are precursors for the formation of cross - links which provide collagen with its tensile strength. |
| Score | Text |
|---|---|
| 0.9988 | No disorder has been directly linked to decreased expression of LH2 and ProteinLH3 , two other isoforms of LH. |
| 0.9988 | No disorder has been directly linked to decreased expression of ProteinLH2 and LH3, two other isoforms of LH. |
| Score | Text |
|---|---|
| 0.9987 | This study describes 3 patients with mixed phenotypes of EDS, who have significantly decreased mRNAs for LH2, but normal levels of LH1 and ProteinLH3 mRNAs, in their skin fibroblasts. |
| 0.9984 | This study describes 3 patients with mixed phenotypes of EDS, who have significantly decreased mRNAs for ProteinLH2 , but normal levels of LH1 and LH3 mRNAs, in their skin fibroblasts. |
| 0.9979 | This study describes 3 patients with mixed phenotypes of EDS, who have significantly decreased mRNAs for LH2, but normal levels of ProteinLH1 and LH3 mRNAs, in their skin fibroblasts. |
| Score | Text |
|---|---|
| 0.9985 | In contrast to the effect of ProteinLH1 deficiency in EDS VI patients, the decreased expression of LH2 does not affect LH activity, bifunctional collagen cross - links ( measured after reduction as dihydroxylysinonorleucine ( DHLNL ) and hydroxylysinonorleucine ( HLNL ) ), or helical lysine hydroxylation in these cell lines. |
| 0.9984 | In contrast to the effect of LH1 deficiency in EDS VI patients, the decreased expression of ProteinLH2 does not affect LH activity, bifunctional collagen cross - links ( measured after reduction as dihydroxylysinonorleucine ( DHLNL ) and hydroxylysinonorleucine ( HLNL ) ), or helical lysine hydroxylation in these cell lines. |
| Score | Text |
|---|---|
| 0.9995 | Sequence analysis of full length LH2 cDNAs and 1kb of the promoter region of ProteinLH2 does not show mutations that could explain the decreased expression of LH2. |
| 0.9995 | Sequence analysis of full length LH2 cDNAs and 1kb of the promoter region of LH2 does not show mutations that could explain the decreased expression of ProteinLH2 . |
| 0.9986 | Sequence analysis of full length ProteinLH2 cDNAs and 1kb of the promoter region of LH2 does not show mutations that could explain the decreased expression of LH2. |
| Score | Text |
|---|---|
| 0.9996 | These results suggest that the deficiency of ProteinLH2 in these fibroblasts may be caused by changes in other factors required for the expression of LH2. |
| 0.9995 | These results suggest that the deficiency of LH2 in these fibroblasts may be caused by changes in other factors required for the expression of ProteinLH2 . |
| Score | Text |
|---|---|
| 0.9998 | Expression and purification of functionally active hyaluronan - binding domains from human cartilage link protein, aggrecan and Proteinversican : formation of ternary complexes with defined hyaluronan oligosaccharides. |
| 0.9995 | Expression and purification of functionally active hyaluronan - binding domains from human cartilage link protein, Proteinaggrecan and versican : formation of ternary complexes with defined hyaluronan oligosaccharides. |
| Score | Text |
|---|---|
| 0.9984 | The chondroitin sulfate proteoglycan Proteinaggrecan forms link protein - stabilized complexes with hyaluronan ( HA ), via its N - terminal G1 - domain, that provide cartilage with its load bearing properties. |
| Score | Text |
|---|---|
| 0.9993 | Similar aggregates ( potentially containing new members of the link protein family ), in which other chondroitin sulfate proteoglycans ( i. e. versican, brevican, and neurocan ) substitute for Proteinaggrecan , may contribute to the structural integrity of many other tissues including skin and brain. |
| 0.9986 | Similar aggregates ( potentially containing new members of the link protein family ), in which other chondroitin sulfate proteoglycans ( i. e. versican, Proteinbrevican , and neurocan ) substitute for aggrecan, may contribute to the structural integrity of many other tissues including skin and brain. |
| 0.9986 | Similar aggregates ( potentially containing new members of the link protein family ), in which other chondroitin sulfate proteoglycans ( i. e. Proteinversican , brevican, and neurocan ) substitute for aggrecan, may contribute to the structural integrity of many other tissues including skin and brain. |
| 0.9984 | Similar aggregates ( potentially containing new members of the link protein family ), in which other chondroitin sulfate proteoglycans ( i. e. versican, brevican, and Proteinneurocan ) substitute for aggrecan, may contribute to the structural integrity of many other tissues including skin and brain. |
| Score | Text |
|---|---|
| 0.9983 | In this study, cartilage link protein ( cLP ) and the G1 - domains of Proteinaggrecan ( AG1 ) and versican ( VG1 ) were expressed in Drosophila S2 cells. |
| 0.9975 | In this study, cartilage link protein ( cLP ) and the G1 - domains of aggrecan ( AG1 ) and Proteinversican ( VG1 ) were expressed in Drosophila S2 cells. |
| Score | Text |
|---|---|
| 0.9383 | The recombinant human proteins were found to have properties similar to those described for the native molecules ( e. g. cLP was able to form oligomers, and ProteinHA decasaccharides were the minimum size that could compete effectively for their binding to polymeric HA ). |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9996 | Surprisingly, the length of HA required to accommodate two G1 - domains was found to be significantly larger for aggrecan than Proteinversican , which may reflect differences in the conformation of HA stabilized on binding these proteins. |
| 0.9995 | Surprisingly, the length of HA required to accommodate two G1 - domains was found to be significantly larger for Proteinaggrecan than versican, which may reflect differences in the conformation of HA stabilized on binding these proteins. |
| Score | Text |
|---|---|
| 0.9968 | Protective mechanism of epigallocatechin - 3 - gallate against Helicobacter pylori - induced gastric epithelial cytotoxicity via the blockage of ProteinTLR - 4 signaling. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9995 | To investigate the effect of EGCG on H. pylori - induced toll - like receptor 4 ( TLR - 4 ) signaling, reverse transcription - polymerase chain reaction and Western blot analysis corresponding to glycosylated ProteinTLR - 4 were carried out. |
| 0.9909 | To investigate the effect of EGCG on H. pylori - induced toll - like receptor 4 ( TLR - 4 ) signaling, reverse transcription - polymerase chain reaction and Western blot analysis corresponding to Glycosylationglycosylated TLR - 4 were carried out. |
| 0.9659 | To investigate the effect of EGCG on H. pylori - induced toll - like receptor 4 Protein( TLR - 4 ) signaling, reverse transcription - polymerase chain reaction and Western blot analysis corresponding to glycosylated TLR - 4 were carried out. |
| 0.7672 | To investigate the effect of EGCG on H. pylori - induced Proteintoll - like receptor 4 ( TLR - 4 ) signaling, reverse transcription - polymerase chain reaction and Western blot analysis corresponding to glycosylated TLR - 4 were carried out. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9991 | Helicobacter pylori infection stimulated the glycosylation of ProteinTLR - 4 , which initiates intracellular signaling in the infected host cell, but the pretreatment with EGCG completely blocked the TLR - 4 glycosylation. |
| 0.9966 | Helicobacter pylori infection stimulated the glycosylation of TLR - 4, which initiates intracellular signaling in the infected host cell, but the pretreatment with EGCG completely blocked the ProteinTLR - 4 glycosylation. |
| 0.9873 | Helicobacter pylori infection stimulated the Glycosylationglycosylation of TLR - 4, which initiates intracellular signaling in the infected host cell, but the pretreatment with EGCG completely blocked the TLR - 4 glycosylation. |
| 0.9561 | Helicobacter pylori infection stimulated the glycosylation of TLR - 4, which initiates intracellular signaling in the infected host cell, but the pretreatment with EGCG completely blocked the TLR - 4 Glycosylationglycosylation . |
| Score | Text |
|---|---|
| 0.9998 | The blockage of ProteinTLR - 4 activation by EGCG resulted in inactivation of extracellular signal response kinase 1 / 2 and of nuclear factor - kappaB, the downstream molecules of TLR - 4 signaling induced by H. pylori. |
| 0.9996 | The blockage of TLR - 4 activation by EGCG resulted in inactivation of extracellular signal response kinase 1 / 2 and of nuclear factor - kappaB, the downstream molecules of ProteinTLR - 4 signaling induced by H. pylori. |
| 0.9632 | The blockage of TLR - 4 activation by EGCG resulted in inactivation of extracellular signal response kinase Protein1 / 2 and of nuclear factor - kappaB, the downstream molecules of TLR - 4 signaling induced by H. pylori. |
| 0.7716 | The blockage of TLR - 4 activation by EGCG resulted in inactivation of Proteinextracellular signal response kinase 1 / 2 and of nuclear factor - kappaB, the downstream molecules of TLR - 4 signaling induced by H. pylori. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9979 | CONCLUSIONS : EGCG pretreatment showed significant cytoprotective effects against H. pylori - induced gastric cytotoxicity via interference of the ProteinTLR - 4 signaling induced by H. pylori. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9966 | Bare - faced curassow Proteinlysozyme carrying amino acid substitutions at subsites E and F shows a change in activity against chitooligosaccharide caused by a local conformational change. |
| Score | Text |
|---|---|
| 0.9737 | A new form of avian lysozyme, bare - faced curassow Proteinlysozyme ( BCL ), was purified and chemically sequenced. |
| Score | Text |
|---|---|
| 0.9986 | Of the 26 substitutions relative to chicken Proteinlysozyme , three, F34Y, T47S, and R114H, are of substrate - interacting residues in the E and F subsites, which would contribute to the acceptor binding for transglycosylation. |
| Score | Text |
|---|---|
| 0.9817 | T47S is a novel substitution in this Proteinlysozyme class. |
| Score | Text |
|---|---|
| 0.9987 | While other Proteinlysozymes also have substitutions at positions 114 and 34, they also contain numerous others, including ones in the other substrate binding sites, A - D. |
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| Score | Text |
|---|---|
| 0.9946 | MD simulation analysis of BCL suggested that the substituted amino acids changed the local conformation of this Proteinlysozyme at the E - F sites. |
| Score | Text |
|---|---|
| 0.9727 | Histone H2B Ubiquitinationubiquitylation is associated with elongating RNA polymerase II. |
| 0.9419 | ProteinHistone H2B ubiquitylation is associated with elongating RNA polymerase II. |
| Score | Text |
|---|---|
| 0.9673 | Rad6 - mediated ubiquitylation of histone H2B at lysine 123 has been linked to transcriptional activation and the regulation of lysine Methylationmethylation on histone H3. |
| 0.9612 | Rad6 - mediated Ubiquitinationubiquitylation of histone H2B at lysine 123 has been linked to transcriptional activation and the regulation of lysine methylation on histone H3. |
| 0.9571 | Rad6 - mediated ubiquitylation of histone H2B at lysine 123 has been linked to transcriptional activation and the regulation of lysine methylation on Proteinhistone H3 . |
| 0.9294 | Rad6 - mediated ubiquitylation of histone H2B at Entitylysine 123 has been linked to transcriptional activation and the regulation of lysine methylation on histone H3. |
| 0.9205 | Rad6 - mediated ubiquitylation of histone H2B at lysine 123 has been linked to transcriptional activation and the regulation of Entitylysine methylation on histone H3. |
| 0.9110 | ProteinRad6 - mediated ubiquitylation of histone H2B at lysine 123 has been linked to transcriptional activation and the regulation of lysine methylation on histone H3. |
| 0.8977 | Rad6 - mediated ubiquitylation of Proteinhistone H2B at lysine 123 has been linked to transcriptional activation and the regulation of lysine methylation on histone H3. |
| 0.5465 | Rad6 - mediated ubiquitylation of histone H2B at Entitylysine 123 has been linked to transcriptional activation and the regulation of lysine methylation on histone H3. |
| Score | Text |
|---|---|
| 0.9952 | However, how ProteinRad6 and H2B ubiquitylation contribute to the transcription and histone methylation processes is poorly understood. |
| 0.9940 | However, how Rad6 and ProteinH2B ubiquitylation contribute to the transcription and histone methylation processes is poorly understood. |
| 0.9820 | However, how Rad6 and H2B ubiquitylation contribute to the transcription and Proteinhistone methylation processes is poorly understood. |
| 0.9460 | However, how Rad6 and H2B Ubiquitinationubiquitylation contribute to the transcription and histone methylation processes is poorly understood. |
| 0.8440 | However, how Rad6 and H2B ubiquitylation contribute to the transcription and histone Methylationmethylation processes is poorly understood. |
| Score | Text |
|---|---|
| 0.9996 | Here, we show that the ProteinPaf1 transcription elongation complex and the E3 ligase for Rad6, Bre1, mediate an association of Rad6 with the hyperphosphorylated ( elongating ) form of RNA polymerase II ( Pol II ). |
| 0.9991 | Here, we show that the Paf1 transcription elongation complex and the E3 ligase for Rad6, ProteinBre1 , mediate an association of Rad6 with the hyperphosphorylated ( elongating ) form of RNA polymerase II ( Pol II ). |
| 0.9991 | Here, we show that the Paf1 transcription elongation complex and the E3 ligase for Rad6, Bre1, mediate an association of ProteinRad6 with the hyperphosphorylated ( elongating ) form of RNA polymerase II ( Pol II ). |
| 0.9979 | Here, we show that the Paf1 transcription elongation complex and the E3 ligase for ProteinRad6 , Bre1, mediate an association of Rad6 with the hyperphosphorylated ( elongating ) form of RNA polymerase II ( Pol II ). |
| 0.6980 | Here, we show that the Paf1 transcription elongation complex and the E3 ligase for Rad6, Bre1, mediate an association of Rad6 with the Phosphorylationhyperphosphorylated ( elongating ) form of RNA polymerase II ( Pol II ). |
| Score | Text |
|---|---|
| 0.9982 | This association appears to be necessary for the transcriptional activities of Rad6, as deletion of various Paf1 complex members or ProteinBre1 abolishes H2B ubiquitylation ( ubH2B ) and reduces the recruitment of Rad6 to the promoters and transcribed regions of active genes. |
| 0.9962 | This association appears to be necessary for the transcriptional activities of Rad6, as deletion of various ProteinPaf1 complex members or Bre1 abolishes H2B ubiquitylation ( ubH2B ) and reduces the recruitment of Rad6 to the promoters and transcribed regions of active genes. |
| 0.9946 | This association appears to be necessary for the transcriptional activities of ProteinRad6 , as deletion of various Paf1 complex members or Bre1 abolishes H2B ubiquitylation ( ubH2B ) and reduces the recruitment of Rad6 to the promoters and transcribed regions of active genes. |
| 0.9924 | This association appears to be necessary for the transcriptional activities of Rad6, as deletion of various Paf1 complex members or Bre1 abolishes H2B ubiquitylation ( ubH2B ) and reduces the recruitment of ProteinRad6 to the promoters and transcribed regions of active genes. |
| 0.9870 | This association appears to be necessary for the transcriptional activities of Rad6, as deletion of various Paf1 complex members or Bre1 abolishes ProteinH2B ubiquitylation ( ubH2B ) and reduces the recruitment of Rad6 to the promoters and transcribed regions of active genes. |
| 0.9690 | This association appears to be necessary for the transcriptional activities of Rad6, as deletion of various Paf1 complex members or Bre1 abolishes H2B Ubiquitinationubiquitylation ( ubH2B ) and reduces the recruitment of Rad6 to the promoters and transcribed regions of active genes. |
| 0.9536 | This association appears to be necessary for the transcriptional activities of Rad6, as deletion of various Paf1 complex members or Bre1 abolishes H2B ubiquitylation Protein( ubH2B ) and reduces the recruitment of Rad6 to the promoters and transcribed regions of active genes. |
| 0.5365 | This association appears to be necessary for the transcriptional activities of Rad6, as deletion of various Paf1 complex members or Bre1 abolishes H2B Ubiquitinationubiquitylation ( ubH2B ) and reduces the recruitment of Rad6 to the promoters and transcribed regions of active genes. |
| Score | Text |
|---|---|
| 0.9999 | Using the inducible ProteinGAL1 gene as a model, we find that the recruitment of Rad6 upon activation occurs rapidly and transiently across the gene and coincides precisely with the appearance of Pol II. |
| 0.9989 | Using the inducible GAL1 gene as a model, we find that the recruitment of ProteinRad6 upon activation occurs rapidly and transiently across the gene and coincides precisely with the appearance of Pol II. |
| Score | Text |
|---|---|
| 0.9997 | Significantly, during ProteinGAL1 activation in an rtf1 deletion mutant, Rad6 accumulates at the promoter but is absent from the transcribed region. |
| 0.9996 | Significantly, during GAL1 activation in an Proteinrtf1 deletion mutant, Rad6 accumulates at the promoter but is absent from the transcribed region. |
| 0.9977 | Significantly, during GAL1 activation in an rtf1 deletion mutant, ProteinRad6 accumulates at the promoter but is absent from the transcribed region. |
| Score | Text |
|---|---|
| 0.9993 | This fact suggests that Rad6 is recruited to promoters independently of the ProteinPaf1 complex but then requires this complex for entrance into the coding region of genes in a Pol II - associated manner. |
| 0.9989 | This fact suggests that ProteinRad6 is recruited to promoters independently of the Paf1 complex but then requires this complex for entrance into the coding region of genes in a Pol II - associated manner. |
| Score | Text |
|---|---|
| 0.9991 | In support of a role for Rad6 - dependent H2B ubiquitylation in transcription elongation, we find that ProteinubH2B levels are dramatically reduced in strains bearing mutations of the Pol II C - terminal domain ( CTD ) and abolished by inactivation of Kin28, the serine 5 CTD kinase that promotes the transition from initiation to elongation. |
| 0.9976 | In support of a role for Rad6 - dependent H2B ubiquitylation in transcription elongation, we find that ubH2B levels are dramatically reduced in strains bearing mutations of the Pol II C - terminal domain ( CTD ) and abolished by inactivation of ProteinKin28 , the serine 5 CTD kinase that promotes the transition from initiation to elongation. |
| 0.9699 | In support of a role for Rad6 - dependent H2B Ubiquitinationubiquitylation in transcription elongation, we find that ubH2B levels are dramatically reduced in strains bearing mutations of the Pol II C - terminal domain ( CTD ) and abolished by inactivation of Kin28, the serine 5 CTD kinase that promotes the transition from initiation to elongation. |
| 0.9572 | In support of a role for Rad6 - dependent ProteinH2B ubiquitylation in transcription elongation, we find that ubH2B levels are dramatically reduced in strains bearing mutations of the Pol II C - terminal domain ( CTD ) and abolished by inactivation of Kin28, the serine 5 CTD kinase that promotes the transition from initiation to elongation. |
| 0.9026 | In support of a role for ProteinRad6 - dependent H2B ubiquitylation in transcription elongation, we find that ubH2B levels are dramatically reduced in strains bearing mutations of the Pol II C - terminal domain ( CTD ) and abolished by inactivation of Kin28, the serine 5 CTD kinase that promotes the transition from initiation to elongation. |
| 0.8137 | In support of a role for ProteinRad6 - dependent H2B ubiquitylation in transcription elongation, we find that ubH2B levels are dramatically reduced in strains bearing mutations of the Pol II C - terminal domain ( CTD ) and abolished by inactivation of Kin28, the serine 5 CTD kinase that promotes the transition from initiation to elongation. |
| Score | Text |
|---|---|
| 0.9979 | Furthermore, synthetic genetic array analysis reveals that the ProteinRad6 complex interacts genetically with a number of known or suspected transcription elongation factors. |
| Score | Text |
|---|---|
| 0.9909 | Finally, we show that Saccharomyces cerevisiae mutants bearing defects in the pathway to ProteinH2B ubiquitylation display transcription elongation defects as assayed by 6 - azauracil sensitivity. |
| 0.9725 | Finally, we show that Saccharomyces cerevisiae mutants bearing defects in the pathway to H2B Ubiquitinationubiquitylation display transcription elongation defects as assayed by 6 - azauracil sensitivity. |
| Score | Text |
|---|---|
| 0.9955 | Collectively, our results indicate a role for Rad6 and H2B ubiquitylation during the elongation cycle of transcription and suggest a mechanism by which ProteinH3 methylation may be regulated. |
| 0.9910 | Collectively, our results indicate a role for Rad6 and ProteinH2B ubiquitylation during the elongation cycle of transcription and suggest a mechanism by which H3 methylation may be regulated. |
| 0.9833 | Collectively, our results indicate a role for ProteinRad6 and H2B ubiquitylation during the elongation cycle of transcription and suggest a mechanism by which H3 methylation may be regulated. |
| 0.9372 | Collectively, our results indicate a role for Rad6 and H2B Ubiquitinationubiquitylation during the elongation cycle of transcription and suggest a mechanism by which H3 methylation may be regulated. |
| 0.8328 | Collectively, our results indicate a role for Rad6 and H2B ubiquitylation during the elongation cycle of transcription and suggest a mechanism by which H3 Methylationmethylation may be regulated. |
| Score | Text |
|---|---|
| 0.9972 | Glycosylation - related gene expression in prion diseases : ProteinPrPSc accumulation in scrapie infected GT1 cells depends on beta - 1, 4 - linked GalNAc - 4 - SO4 hyposulfation. |
| 0.9940 | Glycosylation - related gene expression in Proteinprion diseases : PrPSc accumulation in scrapie infected GT1 cells depends on beta - 1, 4 - linked GalNAc - 4 - SO4 hyposulfation. |